CN115317528A - Application of ginseng fruit total saponin and medicine for resisting myocardial fibrosis - Google Patents
Application of ginseng fruit total saponin and medicine for resisting myocardial fibrosis Download PDFInfo
- Publication number
- CN115317528A CN115317528A CN202210921892.3A CN202210921892A CN115317528A CN 115317528 A CN115317528 A CN 115317528A CN 202210921892 A CN202210921892 A CN 202210921892A CN 115317528 A CN115317528 A CN 115317528A
- Authority
- CN
- China
- Prior art keywords
- myocardial
- fibrosis
- myocardial fibrosis
- total saponins
- collagen
- Prior art date
- Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
- Pending
Links
- 150000007949 saponins Chemical class 0.000 title claims abstract description 49
- 229930182490 saponin Natural products 0.000 title claims abstract description 48
- 235000008434 ginseng Nutrition 0.000 title claims abstract description 47
- 206010028594 Myocardial fibrosis Diseases 0.000 title claims abstract description 42
- 235000013399 edible fruits Nutrition 0.000 title claims abstract description 36
- 241000208340 Araliaceae Species 0.000 title claims abstract description 29
- 235000005035 Panax pseudoginseng ssp. pseudoginseng Nutrition 0.000 title claims abstract description 29
- 235000003140 Panax quinquefolius Nutrition 0.000 title claims abstract description 29
- 239000003814 drug Substances 0.000 title claims abstract description 22
- 239000001397 quillaja saponaria molina bark Substances 0.000 title claims abstract description 12
- 235000017709 saponins Nutrition 0.000 claims description 45
- 230000002107 myocardial effect Effects 0.000 claims description 28
- 108010035532 Collagen Proteins 0.000 claims description 25
- 102000008186 Collagen Human genes 0.000 claims description 25
- 229920001436 collagen Polymers 0.000 claims description 25
- 206010000891 acute myocardial infarction Diseases 0.000 claims description 24
- 240000004371 Panax ginseng Species 0.000 claims description 18
- 235000002789 Panax ginseng Nutrition 0.000 claims description 18
- 230000014509 gene expression Effects 0.000 claims description 11
- 241001465754 Metazoa Species 0.000 claims description 10
- 230000008021 deposition Effects 0.000 claims description 8
- 229940079593 drug Drugs 0.000 claims description 8
- 238000000034 method Methods 0.000 claims description 8
- 239000000835 fiber Substances 0.000 claims description 7
- 230000006378 damage Effects 0.000 claims description 6
- 208000027418 Wounds and injury Diseases 0.000 claims description 5
- 208000014674 injury Diseases 0.000 claims description 5
- 239000000463 material Substances 0.000 claims description 3
- 230000003247 decreasing effect Effects 0.000 claims 1
- 208000010125 myocardial infarction Diseases 0.000 abstract description 11
- 208000037273 Pathologic Processes Diseases 0.000 abstract description 2
- 230000009054 pathological process Effects 0.000 abstract description 2
- 241000699670 Mus sp. Species 0.000 description 16
- 206010016654 Fibrosis Diseases 0.000 description 11
- 230000004761 fibrosis Effects 0.000 description 11
- 230000002861 ventricular Effects 0.000 description 11
- 210000001519 tissue Anatomy 0.000 description 10
- 210000002966 serum Anatomy 0.000 description 9
- 239000002775 capsule Substances 0.000 description 7
- 230000000747 cardiac effect Effects 0.000 description 7
- 210000004165 myocardium Anatomy 0.000 description 7
- 108010022452 Collagen Type I Proteins 0.000 description 6
- 102000012422 Collagen Type I Human genes 0.000 description 6
- 238000001514 detection method Methods 0.000 description 6
- 230000003205 diastolic effect Effects 0.000 description 6
- 102000004169 proteins and genes Human genes 0.000 description 6
- 108090000623 proteins and genes Proteins 0.000 description 6
- LFQSCWFLJHTTHZ-UHFFFAOYSA-N Ethanol Chemical compound CCO LFQSCWFLJHTTHZ-UHFFFAOYSA-N 0.000 description 5
- 206010020772 Hypertension Diseases 0.000 description 5
- 241000699666 Mus <mouse, genus> Species 0.000 description 5
- 238000011161 development Methods 0.000 description 5
- 230000004217 heart function Effects 0.000 description 5
- 210000000651 myofibroblast Anatomy 0.000 description 5
- 208000024172 Cardiovascular disease Diseases 0.000 description 4
- 102000003979 Mineralocorticoid Receptors Human genes 0.000 description 4
- 108090000375 Mineralocorticoid Receptors Proteins 0.000 description 4
- 206010028851 Necrosis Diseases 0.000 description 4
- 206010003119 arrhythmia Diseases 0.000 description 4
- 230000006793 arrhythmia Effects 0.000 description 4
- 210000001054 cardiac fibroblast Anatomy 0.000 description 4
- 210000000038 chest Anatomy 0.000 description 4
- 239000003112 inhibitor Substances 0.000 description 4
- 208000028867 ischemia Diseases 0.000 description 4
- 238000005259 measurement Methods 0.000 description 4
- 230000017074 necrotic cell death Effects 0.000 description 4
- 235000018102 proteins Nutrition 0.000 description 4
- 229940044551 receptor antagonist Drugs 0.000 description 4
- 239000002464 receptor antagonist Substances 0.000 description 4
- 230000009467 reduction Effects 0.000 description 4
- 238000010186 staining Methods 0.000 description 4
- 238000002604 ultrasonography Methods 0.000 description 4
- 238000001262 western blot Methods 0.000 description 4
- PIWKPBJCKXDKJR-UHFFFAOYSA-N Isoflurane Chemical compound FC(F)OC(Cl)C(F)(F)F PIWKPBJCKXDKJR-UHFFFAOYSA-N 0.000 description 3
- 230000002411 adverse Effects 0.000 description 3
- 210000004027 cell Anatomy 0.000 description 3
- KRKNYBCHXYNGOX-UHFFFAOYSA-N citric acid Chemical compound OC(=O)CC(O)(C(O)=O)CC(O)=O KRKNYBCHXYNGOX-UHFFFAOYSA-N 0.000 description 3
- 201000010099 disease Diseases 0.000 description 3
- 208000037265 diseases, disorders, signs and symptoms Diseases 0.000 description 3
- 238000002474 experimental method Methods 0.000 description 3
- 230000006870 function Effects 0.000 description 3
- 229930182494 ginsenoside Natural products 0.000 description 3
- 229940089161 ginsenoside Drugs 0.000 description 3
- 206010020871 hypertrophic cardiomyopathy Diseases 0.000 description 3
- 230000000302 ischemic effect Effects 0.000 description 3
- 229960002725 isoflurane Drugs 0.000 description 3
- 230000003907 kidney function Effects 0.000 description 3
- 210000004185 liver Anatomy 0.000 description 3
- 230000003680 myocardial damage Effects 0.000 description 3
- 231100000915 pathological change Toxicity 0.000 description 3
- 230000036285 pathological change Effects 0.000 description 3
- 230000001575 pathological effect Effects 0.000 description 3
- 239000000843 powder Substances 0.000 description 3
- 230000036454 renin-angiotensin system Effects 0.000 description 3
- 239000005541 ACE inhibitor Substances 0.000 description 2
- 102100036475 Alanine aminotransferase 1 Human genes 0.000 description 2
- 108010082126 Alanine transaminase Proteins 0.000 description 2
- IJGRMHOSHXDMSA-UHFFFAOYSA-N Atomic nitrogen Chemical compound N#N IJGRMHOSHXDMSA-UHFFFAOYSA-N 0.000 description 2
- 239000002083 C09CA01 - Losartan Substances 0.000 description 2
- 229940127291 Calcium channel antagonist Drugs 0.000 description 2
- 206010052337 Diastolic dysfunction Diseases 0.000 description 2
- 238000002965 ELISA Methods 0.000 description 2
- 229940118365 Endothelin receptor antagonist Drugs 0.000 description 2
- 206010019280 Heart failures Diseases 0.000 description 2
- 108091005975 Myofilaments Proteins 0.000 description 2
- WHNWPMSKXPGLAX-UHFFFAOYSA-N N-Vinyl-2-pyrrolidone Chemical compound C=CN1CCCC1=O WHNWPMSKXPGLAX-UHFFFAOYSA-N 0.000 description 2
- 206010042434 Sudden death Diseases 0.000 description 2
- 239000004480 active ingredient Substances 0.000 description 2
- 239000002671 adjuvant Substances 0.000 description 2
- 229940127282 angiotensin receptor antagonist Drugs 0.000 description 2
- 229940044094 angiotensin-converting-enzyme inhibitor Drugs 0.000 description 2
- 239000003963 antioxidant agent Substances 0.000 description 2
- 239000002876 beta blocker Substances 0.000 description 2
- 238000001574 biopsy Methods 0.000 description 2
- 210000004369 blood Anatomy 0.000 description 2
- 239000008280 blood Substances 0.000 description 2
- 210000004413 cardiac myocyte Anatomy 0.000 description 2
- 230000008859 change Effects 0.000 description 2
- 208000029078 coronary artery disease Diseases 0.000 description 2
- 210000004351 coronary vessel Anatomy 0.000 description 2
- DDRJAANPRJIHGJ-UHFFFAOYSA-N creatinine Chemical compound CN1CC(=O)NC1=N DDRJAANPRJIHGJ-UHFFFAOYSA-N 0.000 description 2
- 239000002552 dosage form Substances 0.000 description 2
- 230000002526 effect on cardiovascular system Effects 0.000 description 2
- 230000000694 effects Effects 0.000 description 2
- 239000002308 endothelin receptor antagonist Substances 0.000 description 2
- 238000005516 engineering process Methods 0.000 description 2
- 208000019622 heart disease Diseases 0.000 description 2
- 238000007490 hematoxylin and eosin (H&E) staining Methods 0.000 description 2
- 230000001631 hypertensive effect Effects 0.000 description 2
- 230000008595 infiltration Effects 0.000 description 2
- 238000001764 infiltration Methods 0.000 description 2
- 210000004969 inflammatory cell Anatomy 0.000 description 2
- 230000003601 intercostal effect Effects 0.000 description 2
- 230000003908 liver function Effects 0.000 description 2
- KJJZZJSZUJXYEA-UHFFFAOYSA-N losartan Chemical compound CCCCC1=NC(Cl)=C(CO)N1CC1=CC=C(C=2C(=CC=CC=2)C=2[N]N=NN=2)C=C1 KJJZZJSZUJXYEA-UHFFFAOYSA-N 0.000 description 2
- 229960004773 losartan Drugs 0.000 description 2
- 210000003632 microfilament Anatomy 0.000 description 2
- 210000003205 muscle Anatomy 0.000 description 2
- 208000031225 myocardial ischemia Diseases 0.000 description 2
- 210000001087 myotubule Anatomy 0.000 description 2
- 238000007634 remodeling Methods 0.000 description 2
- 230000008439 repair process Effects 0.000 description 2
- 230000000405 serological effect Effects 0.000 description 2
- 229960002256 spironolactone Drugs 0.000 description 2
- LXMSZDCAJNLERA-ZHYRCANASA-N spironolactone Chemical compound C([C@@H]1[C@]2(C)CC[C@@H]3[C@@]4(C)CCC(=O)C=C4C[C@H]([C@@H]13)SC(=O)C)C[C@@]21CCC(=O)O1 LXMSZDCAJNLERA-ZHYRCANASA-N 0.000 description 2
- 210000000115 thoracic cavity Anatomy 0.000 description 2
- XLYOFNOQVPJJNP-UHFFFAOYSA-N water Substances O XLYOFNOQVPJJNP-UHFFFAOYSA-N 0.000 description 2
- NIXOWILDQLNWCW-UHFFFAOYSA-N Acrylic acid Chemical compound OC(=O)C=C NIXOWILDQLNWCW-UHFFFAOYSA-N 0.000 description 1
- 102000007469 Actins Human genes 0.000 description 1
- 108010085238 Actins Proteins 0.000 description 1
- 229910002012 Aerosil® Inorganic materials 0.000 description 1
- PQSUYGKTWSAVDQ-ZVIOFETBSA-N Aldosterone Chemical compound C([C@@]1([C@@H](C(=O)CO)CC[C@H]1[C@@H]1CC2)C=O)[C@H](O)[C@@H]1[C@]1(C)C2=CC(=O)CC1 PQSUYGKTWSAVDQ-ZVIOFETBSA-N 0.000 description 1
- PQSUYGKTWSAVDQ-UHFFFAOYSA-N Aldosterone Natural products C1CC2C3CCC(C(=O)CO)C3(C=O)CC(O)C2C2(C)C1=CC(=O)CC2 PQSUYGKTWSAVDQ-UHFFFAOYSA-N 0.000 description 1
- 206010002091 Anaesthesia Diseases 0.000 description 1
- 238000011740 C57BL/6 mouse Methods 0.000 description 1
- 206010007558 Cardiac failure chronic Diseases 0.000 description 1
- 206010007559 Cardiac failure congestive Diseases 0.000 description 1
- 206010007572 Cardiac hypertrophy Diseases 0.000 description 1
- 208000031229 Cardiomyopathies Diseases 0.000 description 1
- 229920001661 Chitosan Polymers 0.000 description 1
- JZUFKLXOESDKRF-UHFFFAOYSA-N Chlorothiazide Chemical compound C1=C(Cl)C(S(=O)(=O)N)=CC2=C1NCNS2(=O)=O JZUFKLXOESDKRF-UHFFFAOYSA-N 0.000 description 1
- 102100036213 Collagen alpha-2(I) chain Human genes 0.000 description 1
- 208000002330 Congenital Heart Defects Diseases 0.000 description 1
- 206010056370 Congestive cardiomyopathy Diseases 0.000 description 1
- 102000004420 Creatine Kinase Human genes 0.000 description 1
- 108010042126 Creatine kinase Proteins 0.000 description 1
- FBPFZTCFMRRESA-KVTDHHQDSA-N D-Mannitol Chemical compound OC[C@@H](O)[C@@H](O)[C@H](O)[C@H](O)CO FBPFZTCFMRRESA-KVTDHHQDSA-N 0.000 description 1
- 229920001353 Dextrin Polymers 0.000 description 1
- 239000004375 Dextrin Substances 0.000 description 1
- 201000010046 Dilated cardiomyopathy Diseases 0.000 description 1
- 102000010834 Extracellular Matrix Proteins Human genes 0.000 description 1
- 108010037362 Extracellular Matrix Proteins Proteins 0.000 description 1
- 229910052688 Gadolinium Inorganic materials 0.000 description 1
- 208000000435 Heart Rupture Diseases 0.000 description 1
- 101000875067 Homo sapiens Collagen alpha-2(I) chain Proteins 0.000 description 1
- 229920002153 Hydroxypropyl cellulose Polymers 0.000 description 1
- 206010021118 Hypotonia Diseases 0.000 description 1
- 206010021143 Hypoxia Diseases 0.000 description 1
- 206010061218 Inflammation Diseases 0.000 description 1
- 108010007859 Lisinopril Proteins 0.000 description 1
- 229930195725 Mannitol Natural products 0.000 description 1
- 208000001145 Metabolic Syndrome Diseases 0.000 description 1
- 229920000168 Microcrystalline cellulose Polymers 0.000 description 1
- 229920000881 Modified starch Polymers 0.000 description 1
- 208000009525 Myocarditis Diseases 0.000 description 1
- 229930040373 Paraformaldehyde Natural products 0.000 description 1
- 102000035195 Peptidases Human genes 0.000 description 1
- 108091005804 Peptidases Proteins 0.000 description 1
- 239000002202 Polyethylene glycol Substances 0.000 description 1
- 239000004365 Protease Substances 0.000 description 1
- 206010038748 Restrictive cardiomyopathy Diseases 0.000 description 1
- 240000003801 Sigesbeckia orientalis Species 0.000 description 1
- 235000003407 Sigesbeckia orientalis Nutrition 0.000 description 1
- VYPSYNLAJGMNEJ-UHFFFAOYSA-N Silicium dioxide Chemical compound O=[Si]=O VYPSYNLAJGMNEJ-UHFFFAOYSA-N 0.000 description 1
- FAPWRFPIFSIZLT-UHFFFAOYSA-M Sodium chloride Chemical compound [Na+].[Cl-] FAPWRFPIFSIZLT-UHFFFAOYSA-M 0.000 description 1
- 229920002125 Sokalan® Polymers 0.000 description 1
- 229920002472 Starch Polymers 0.000 description 1
- 206010071436 Systolic dysfunction Diseases 0.000 description 1
- 208000033774 Ventricular Remodeling Diseases 0.000 description 1
- 201000000690 abdominal obesity-metabolic syndrome Diseases 0.000 description 1
- 238000009825 accumulation Methods 0.000 description 1
- DPXJVFZANSGRMM-UHFFFAOYSA-N acetic acid;2,3,4,5,6-pentahydroxyhexanal;sodium Chemical compound [Na].CC(O)=O.OCC(O)C(O)C(O)C(O)C=O DPXJVFZANSGRMM-UHFFFAOYSA-N 0.000 description 1
- 230000004913 activation Effects 0.000 description 1
- 239000000853 adhesive Substances 0.000 description 1
- 230000001070 adhesive effect Effects 0.000 description 1
- 229960002478 aldosterone Drugs 0.000 description 1
- 230000037005 anaesthesia Effects 0.000 description 1
- 230000003042 antagnostic effect Effects 0.000 description 1
- 230000003510 anti-fibrotic effect Effects 0.000 description 1
- 206010002906 aortic stenosis Diseases 0.000 description 1
- 238000003556 assay Methods 0.000 description 1
- 229940097320 beta blocking agent Drugs 0.000 description 1
- 230000036770 blood supply Effects 0.000 description 1
- 210000004204 blood vessel Anatomy 0.000 description 1
- 230000037396 body weight Effects 0.000 description 1
- 210000004899 c-terminal region Anatomy 0.000 description 1
- -1 calcium antagonists Substances 0.000 description 1
- 229960001631 carbomer Drugs 0.000 description 1
- 239000001768 carboxy methyl cellulose Substances 0.000 description 1
- 230000007211 cardiovascular event Effects 0.000 description 1
- 230000007012 clinical effect Effects 0.000 description 1
- 208000028831 congenital heart disease Diseases 0.000 description 1
- 210000002808 connective tissue Anatomy 0.000 description 1
- 230000008602 contraction Effects 0.000 description 1
- 239000006071 cream Substances 0.000 description 1
- 229940109239 creatinine Drugs 0.000 description 1
- 229960000913 crospovidone Drugs 0.000 description 1
- 238000005520 cutting process Methods 0.000 description 1
- 210000000805 cytoplasm Anatomy 0.000 description 1
- 230000034994 death Effects 0.000 description 1
- 230000002951 depilatory effect Effects 0.000 description 1
- 235000019425 dextrin Nutrition 0.000 description 1
- 206010012601 diabetes mellitus Diseases 0.000 description 1
- 230000004069 differentiation Effects 0.000 description 1
- 238000007599 discharging Methods 0.000 description 1
- 239000002270 dispersing agent Substances 0.000 description 1
- 238000001035 drying Methods 0.000 description 1
- 230000004064 dysfunction Effects 0.000 description 1
- 238000002592 echocardiography Methods 0.000 description 1
- 239000012636 effector Substances 0.000 description 1
- 230000002349 favourable effect Effects 0.000 description 1
- 238000001914 filtration Methods 0.000 description 1
- UIWYJDYFSGRHKR-UHFFFAOYSA-N gadolinium atom Chemical compound [Gd] UIWYJDYFSGRHKR-UHFFFAOYSA-N 0.000 description 1
- 238000003304 gavage Methods 0.000 description 1
- PWAOOJDMFUQOKB-WCZZMFLVSA-N ginsenoside Re Chemical compound O[C@@H]1[C@H](O)[C@@H](O)[C@H](C)O[C@H]1O[C@H]1[C@H](O[C@@H]2[C@H]3C(C)(C)[C@@H](O)CC[C@]3(C)[C@@H]3[C@@]([C@@]4(CC[C@@H]([C@H]4[C@H](O)C3)[C@](C)(CCC=C(C)C)O[C@H]3[C@@H]([C@@H](O)[C@H](O)[C@@H](CO)O3)O)C)(C)C2)O[C@H](CO)[C@@H](O)[C@@H]1O PWAOOJDMFUQOKB-WCZZMFLVSA-N 0.000 description 1
- AOGZLQUEBLOQCI-UHFFFAOYSA-N ginsenoside-Re Natural products CC1OC(OCC2OC(OC3CC4(C)C(CC(O)C5C(CCC45C)C(C)(CCC=C(C)C)OC6OC(CO)C(O)C(O)C6O)C7(C)CCC(O)C(C)(C)C37)C(O)C(O)C2O)C(O)C(O)C1O AOGZLQUEBLOQCI-UHFFFAOYSA-N 0.000 description 1
- 239000008187 granular material Substances 0.000 description 1
- 230000002439 hemostatic effect Effects 0.000 description 1
- 229960002003 hydrochlorothiazide Drugs 0.000 description 1
- 239000001863 hydroxypropyl cellulose Substances 0.000 description 1
- 235000010977 hydroxypropyl cellulose Nutrition 0.000 description 1
- 201000001421 hyperglycemia Diseases 0.000 description 1
- 230000007954 hypoxia Effects 0.000 description 1
- 238000003384 imaging method Methods 0.000 description 1
- 230000006872 improvement Effects 0.000 description 1
- 230000004054 inflammatory process Effects 0.000 description 1
- 238000001802 infusion Methods 0.000 description 1
- 230000005764 inhibitory process Effects 0.000 description 1
- 238000003780 insertion Methods 0.000 description 1
- 230000037431 insertion Effects 0.000 description 1
- 230000002427 irreversible effect Effects 0.000 description 1
- 210000003734 kidney Anatomy 0.000 description 1
- 210000005240 left ventricle Anatomy 0.000 description 1
- 239000007788 liquid Substances 0.000 description 1
- RLAWWYSOJDYHDC-BZSNNMDCSA-N lisinopril Chemical compound C([C@H](N[C@@H](CCCCN)C(=O)N1[C@@H](CCC1)C(O)=O)C(O)=O)CC1=CC=CC=C1 RLAWWYSOJDYHDC-BZSNNMDCSA-N 0.000 description 1
- 229960002394 lisinopril Drugs 0.000 description 1
- 230000003211 malignant effect Effects 0.000 description 1
- 239000000594 mannitol Substances 0.000 description 1
- 235000010355 mannitol Nutrition 0.000 description 1
- 239000003550 marker Substances 0.000 description 1
- 239000011159 matrix material Substances 0.000 description 1
- 230000007246 mechanism Effects 0.000 description 1
- 239000008108 microcrystalline cellulose Substances 0.000 description 1
- 229940016286 microcrystalline cellulose Drugs 0.000 description 1
- 235000019813 microcrystalline cellulose Nutrition 0.000 description 1
- 238000012986 modification Methods 0.000 description 1
- 230000004048 modification Effects 0.000 description 1
- 238000010172 mouse model Methods 0.000 description 1
- 230000036640 muscle relaxation Effects 0.000 description 1
- 208000037891 myocardial injury Diseases 0.000 description 1
- 210000000107 myocyte Anatomy 0.000 description 1
- 229910052757 nitrogen Inorganic materials 0.000 description 1
- 231100001092 no hepatotoxicity Toxicity 0.000 description 1
- 231100001095 no nephrotoxicity Toxicity 0.000 description 1
- 230000002018 overexpression Effects 0.000 description 1
- 229920002866 paraformaldehyde Polymers 0.000 description 1
- 239000000546 pharmaceutical excipient Substances 0.000 description 1
- 229940124531 pharmaceutical excipient Drugs 0.000 description 1
- 239000006187 pill Substances 0.000 description 1
- 210000004224 pleura Anatomy 0.000 description 1
- 229920001223 polyethylene glycol Polymers 0.000 description 1
- 235000013809 polyvinylpolypyrrolidone Nutrition 0.000 description 1
- 229920000523 polyvinylpolypyrrolidone Polymers 0.000 description 1
- 229920000036 polyvinylpyrrolidone Polymers 0.000 description 1
- 235000013855 polyvinylpyrrolidone Nutrition 0.000 description 1
- 230000002980 postoperative effect Effects 0.000 description 1
- 229940069328 povidone Drugs 0.000 description 1
- 238000002360 preparation method Methods 0.000 description 1
- 238000004393 prognosis Methods 0.000 description 1
- 238000010298 pulverizing process Methods 0.000 description 1
- 238000011160 research Methods 0.000 description 1
- 239000011347 resin Substances 0.000 description 1
- 229920005989 resin Polymers 0.000 description 1
- 230000004044 response Effects 0.000 description 1
- 208000004124 rheumatic heart disease Diseases 0.000 description 1
- 230000036573 scar formation Effects 0.000 description 1
- 230000037390 scarring Effects 0.000 description 1
- 230000003248 secreting effect Effects 0.000 description 1
- 230000028327 secretion Effects 0.000 description 1
- 238000004904 shortening Methods 0.000 description 1
- 235000019812 sodium carboxymethyl cellulose Nutrition 0.000 description 1
- 229920001027 sodium carboxymethylcellulose Polymers 0.000 description 1
- 238000001179 sorption measurement Methods 0.000 description 1
- 239000008107 starch Substances 0.000 description 1
- 235000019698 starch Nutrition 0.000 description 1
- 238000004659 sterilization and disinfection Methods 0.000 description 1
- 230000000638 stimulation Effects 0.000 description 1
- 238000003860 storage Methods 0.000 description 1
- 239000004094 surface-active agent Substances 0.000 description 1
- 230000004083 survival effect Effects 0.000 description 1
- 239000003826 tablet Substances 0.000 description 1
- 238000012360 testing method Methods 0.000 description 1
- 229940126585 therapeutic drug Drugs 0.000 description 1
- 210000000779 thoracic wall Anatomy 0.000 description 1
- 231100000331 toxic Toxicity 0.000 description 1
- 230000002588 toxic effect Effects 0.000 description 1
- 238000005406 washing Methods 0.000 description 1
- 230000003442 weekly effect Effects 0.000 description 1
- 238000005303 weighing Methods 0.000 description 1
- 229940126673 western medicines Drugs 0.000 description 1
- 239000000080 wetting agent Substances 0.000 description 1
Images
Classifications
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K36/00—Medicinal preparations of undetermined constitution containing material from algae, lichens, fungi or plants, or derivatives thereof, e.g. traditional herbal medicines
- A61K36/18—Magnoliophyta (angiosperms)
- A61K36/185—Magnoliopsida (dicotyledons)
- A61K36/25—Araliaceae (Ginseng family), e.g. ivy, aralia, schefflera or tetrapanax
- A61K36/258—Panax (ginseng)
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P9/00—Drugs for disorders of the cardiovascular system
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
- A61P9/00—Drugs for disorders of the cardiovascular system
- A61P9/10—Drugs for disorders of the cardiovascular system for treating ischaemic or atherosclerotic diseases, e.g. antianginal drugs, coronary vasodilators, drugs for myocardial infarction, retinopathy, cerebrovascula insufficiency, renal arteriosclerosis
Landscapes
- Health & Medical Sciences (AREA)
- Natural Medicines & Medicinal Plants (AREA)
- Engineering & Computer Science (AREA)
- Life Sciences & Earth Sciences (AREA)
- Chemical & Material Sciences (AREA)
- Pharmacology & Pharmacy (AREA)
- Bioinformatics & Cheminformatics (AREA)
- Veterinary Medicine (AREA)
- Public Health (AREA)
- General Health & Medical Sciences (AREA)
- Medicinal Chemistry (AREA)
- Animal Behavior & Ethology (AREA)
- Nuclear Medicine, Radiotherapy & Molecular Imaging (AREA)
- Heart & Thoracic Surgery (AREA)
- Organic Chemistry (AREA)
- Cardiology (AREA)
- General Chemical & Material Sciences (AREA)
- Chemical Kinetics & Catalysis (AREA)
- Biotechnology (AREA)
- Vascular Medicine (AREA)
- Alternative & Traditional Medicine (AREA)
- Urology & Nephrology (AREA)
- Botany (AREA)
- Medical Informatics (AREA)
- Microbiology (AREA)
- Mycology (AREA)
- Epidemiology (AREA)
- Steroid Compounds (AREA)
- Medicines Containing Plant Substances (AREA)
Abstract
The invention discloses application of ginseng fruit total saponin in preparing a medicament for resisting myocardial fibrosis and a medicament for resisting myocardial fibrosis. The invention adopts the ginseng fruit total saponin to prepare a safe and effective treatment medicament, and can inhibit the pathological process of myocardial fibrosis after myocardial infarction.
Description
Technical Field
The invention relates to the field of cardiovascular disease drugs, in particular to application of total saponins of ginseng fruit and drugs for resisting myocardial fibrosis.
Background
Myocardial fibrosis is a common pathological link in the development of various cardiovascular diseases (such as myocardial infarction, hypertension, cardiomyopathy and valvular diseases) to the later stage and is an important reason for the continuous development and the irreversible reversion of ventricular remodeling. The continued development of myocardial fibrosis can severely affect the normal systolic and diastolic function of the heart, ultimately leading to chronic heart failure, myocardial infarction, malignant arrhythmia and even sudden death. Myocardial fibrosis is closely related to the prognosis of cardiovascular disease.
At present, inhibitors of the renin-angiotensin-aldosterone system are the primary drugs for the treatment of myocardial fibrosis. In a study of 34 hypertensive patients, endocardial biopsy revealed a reduction in both left ventricular stiffness and fibrosis in patients receiving losartan treatment. Another biopsy study found that lisinopril reduced the cardiac collagen volume fraction compared to hydrochlorothiazide. Cardiac nmr showed that late gadolinium enhancement was significantly reduced in a group of losartan-treated hypertrophic cardiomyopathy patients, suggesting that RAAS inhibitors may inhibit fibrosis. Aldosterone receptor antagonists have a similar anti-myocardial fibrosis effect. Spironolactone can restore the normal collagen content in a mouse model of hypertrophic cardiomyopathy by antagonizing aldosterone. In addition, aldosterone receptor antagonists have a favorable clinical effect in a variety of diseases associated with myocardial scarring such as congestive heart failure, hypertension, coronary heart disease. Spirolactone can reduce the content of C-terminal propeptide and amino-terminal propeptide of serum type I procollagen and improve the diastolic function of the left ventricle in 80 patients with metabolic syndrome. After the patients with failure are treated by the optimal medicament comprising the inhibitor of the renin-angiotensin-aldosterone system in the clinical practice center, the survival rate is still lower for 5 years, and obvious myocardial fibrosis still exists, which indicates that the myocardial fibrosis cannot be well improved by only depending on the inhibition of the renin-angiotensin-aldosterone system.
Therefore, the invention is provided.
Disclosure of Invention
The invention aims to provide application of ginseng fruit total saponin and a medicine for resisting myocardial fibrosis, and aims to solve the problem that medicines in the related art cannot well improve myocardial fibrosis after myocardial infarction.
In order to solve the above problems, in a first aspect, an embodiment of the present invention provides an application of total saponins of panax ginseng in preparing a medicament for resisting myocardial fibrosis, wherein the medicament takes total saponins of panax ginseng as an effective component for resisting myocardial fibrosis.
Further, the myocardial fibrosis includes acute myocardial infarction-induced myocardial histopathological injury.
Further, the acute myocardial infarction-induced myocardial histopathological injury includes myocardial collagen fiber deposition after an acute myocardial infarction.
Further, the anti-myocardial fibrosis includes reducing the expression of myocardial alpha-SMA, collagen I and Collagen III.
Furthermore, the animal dosage of the total saponins of panax ginseng is 19.5mg/kg/d to 39mg/kg/d.
Further, the animal administration amount of the total saponins of panax ginseng fruits is 39mg/kg/d of high dose or 19.5mg/kg/d of low dose.
The total saponins of herba Herminii can be obtained by removing the capsule from the vibration source capsule and retaining the powder therein. The following method may also be employed: taking the ginseng fruit pulp, centrifuging, and centrifuging the centrifugate for later use. Extracting the centrifuged pomace with water, and filtering the extractive solution for later use. Adsorbing centrifugate and extractive solution with macroporous resin column, washing with water after adsorption saturation, eluting with ethanol solution, recovering ethanol from eluate under reduced pressure, collecting eluate, drying under reduced pressure, and pulverizing.
In a second aspect, the embodiments of the present invention further provide a medicament for resisting myocardial fibrosis, which comprises a therapeutically effective amount of total saponins of panax ginseng fruits and pharmaceutical excipients. The adjuvant includes, but is not limited to, an adhesive, a wetting agent, a dispersing agent, a surfactant, etc., and more specifically, may include, but is not limited to, the following conventional adjuvants: starch, dextrin, pregelatinized starch, microcrystalline cellulose, hydroxypropyl cellulose, chitosan, carbomer, sodium carboxymethylcellulose, povidone, polyethylene glycol, crospovidone, aerosil, citric acid, mannitol, etc. The dosage forms prepared by adding auxiliary materials comprise but are not limited to pills, tablets, capsules, granules and other appropriate conventional dosage forms.
Furthermore, the animal dosage of the total saponins of panax ginseng is 19.5mg/kg/d to 39mg/kg/d.
Further, the animal administration amount of the total saponins of panax ginseng fruits is 39mg/kg/d of high dose or 19.5mg/kg/d of low dose.
Compared with the prior art, the invention adopts the ginseng fruit total saponin to prepare a safe and effective treatment medicament, and can inhibit the pathological process of myocardial fibrosis after myocardial infarction.
Drawings
FIG. 1A is a plan view of representative cardiac ultrasounds in groups of mice 2 weeks after acute myocardial infarction;
FIG. 1B is a plan view of typical cardiac ultrasonography measurements in groups of mice 4 weeks after acute myocardial infarction;
FIG. 2 is a graph showing the results of the expression levels of CK-MB, ALT and S-cr in the sera of various groups of mice;
FIG. 3 is a graph of the results of HE staining of myocardial tissues of each group (. Times.400);
FIG. 4 is a graph of Masson staining results (200 times) for each group of myocardial tissues;
FIG. 5 is a graph showing the results of measurement of myocardial CVF in mice of each group;
FIG. 6 is a graph showing the results of expression of myocardial α -SMA, collagen I and Collagen III.
Detailed Description
The principles and spirit of the present invention will be described with reference to a number of exemplary embodiments shown in the drawings. It should be understood that these embodiments are described only to enable those skilled in the art to better understand and to implement the present invention, and are not intended to limit the scope of the present invention in any way.
Myocardial fibrosis refers to excessive deposition of collagen fibers in a normal tissue structure of a cardiac muscle caused by various reasons, wherein the collagen concentration and the collagen volume fraction are remarkably increased, and various types of collagen are in imbalance proportion, so that the structural disorder, the stiffness increase and the ventricular diastolic dysfunction of the cardiac muscle are caused. It is a common pathological change in the development of many cardiovascular and related diseases to a certain stage. Myocardial infarction can cause massive necrosis of billions of myocardial cells in a short time. Since human cardiomyocytes are rarely regenerated, massive cardiomyocyte death results in repair fibrosis to maintain the integrity of the infarcted ventricular structure and prevent cardiac rupture, but excessive myocardial fibrosis can lead to adverse cardiovascular events.
In addition, myocardial fibrosis is a common pathological change in the development of most cardiovascular diseases to a stage often accompanied by systolic and diastolic dysfunction, arrhythmia and cardiovascular adverse events. Myocardial fibrosis can affect cardiac function in several ways, such as perivascular fibrosis can affect coronary blood supply, leading to ischemia, hypoxia and even necrosis of myocardial tissues; the great deposition of collagen fibers leads to the obvious increase of the hardness of the wall of the chamber, the reduction of the compliance, the reduction of the cardiac muscle relaxation and the synchronism, and the reduction of the cardiac function; the massive deposition of collagen fibers in the interstitium can affect the conduction of myocardial electrical signals, and easily form reentry loops, conduction blocks and the like, thereby causing arrhythmia. Myocardial fibrosis can ultimately lead to refractory heart failure, myocardial infarction, arrhythmia and even sudden death.
Myocardial fibrosis occurs in various degrees in many heart diseases such as hypertensive myocardial hypertrophy, myocardial remodeling after coronary heart disease and myocardial infarction, diabetic heart disease, restrictive cardiomyopathy, dilated cardiomyopathy, rheumatic heart disease, congenital heart disease, and the like. Myocardial fibrosis is classified into reactive fibrosis and repair fibrosis according to the presence or absence of myocardial cell necrosis and scar formation. Reactive fibrosis occurs around blood vessels or in the interstitium of the myocardium, and is the reaction of the myocardium to overload, and is commonly seen in hypertension, hypertrophic cardiomyopathy, aortic stenosis, hyperglycemia, and the like; prosthetic fibrosis is a response to myocyte necrosis, commonly seen in myocardial infarction, myocarditis, and the like.
As mentioned above, no targeted therapeutic drug has been found at present because the mechanism of occurrence of myocardial interstitial fibrosis is very complex. The research of the current western medicines mainly focuses on angiotensin converting enzyme inhibitors, angiotensin receptor antagonists, endothelin receptor antagonists, aldosterone receptor antagonists, antioxidants, calcium antagonists, beta-receptor blockers, and the like. Among these drugs, studies of only angiotensin converting enzyme inhibitors and angiotensin receptor antagonists have been strongly documented, but they have not been able to completely inhibit the occurrence of myocardial interstitial fibrosis. Endothelin receptor antagonists, antioxidants are still in the experimental stage, and whether calcium antagonists, aldosterone receptor antagonists, beta-blockers have anti-fibrotic effects remains controversial.
Based on the above, the embodiment of the invention provides an anti-myocardial fibrosis drug, the active ingredient is total saponins of ginseng fruit, in the following embodiment, the source of the total saponins of ginseng fruit is a vibration source capsule (batch number: national standard character Z22026091), wherein only the powder in the capsule is removed, namely the total saponins of ginseng fruit, and after the capsule is collected in a container, the drug taking the total saponins of ginseng fruit as the active ingredient is obtained by weighing according to the specific dosage below.
Animal experimental methods and data
1 method of experiment
Establishing a C57BL/6 mouse acute myocardial infarction model, continuously intragastrically administering the total saponins of ginseng fruit for 4 weeks, performing heart ultrasonic detection on the heart function of the mouse, taking materials, performing histopathological detection, detecting the serological indexes of the mouse by adopting an ELISA method, and detecting the expression of heart-related proteins and genes of the mouse by Western blot and qRCR technologies.
1.1 preparation of mouse acute myocardial infarction model
According to the pre-modeling method of the subject group, a mouse acute myocardial infarction model prepared by adopting the technology of ligating the anterior descending branch of the left coronary artery induces the occurrence of myocardial fibrosis, and the method comprises the following specific steps:
(1) Anesthesia and disinfection: depilatory cream was used to depilate the neck and chest of mice, isoflurane was continuously ventilated and anesthetized, the mice were fixed on the operating table in supine position, and neck and chest were sterilized with 75% alcohol.
(2) Opening the chest: cutting skin at the 3 rd to 4 th intercostal apex of the left side with the length of 1-2cm, separating hypodermis and chest wall muscle layer by layer, and exposing ribs. And slightly opening the intercostal space by using hemostatic forceps, breaking the pleura, fully exposing the heart, slightly squeezing the right chest, and quickly squeezing out the heart along the apex direction.
(3) Ligation: parallel to the anterior inferior corner of the left auricle, at the 1/3 projection position on the anterior descending branch of the left coronary artery, ligating the anterior descending branch with 8-0 suture needle, with the depth of insertion controlled at 1-2mm and the width at about 1.5 mm.
(4) Resetting and suturing: rapidly resetting heart, discharging air from thoracic cavity, closing thoracic layer by layer, and suturing skin with 6-0 suture needle. The mice were placed in an environment of 30 ℃ for resuscitation.
The operation of the sham operation group was the same as that of the model group except that the anterior descending branch was not ligated after the needle was inserted.
1.2 animal grouping and administration
The mice with successfully modeled acute myocardial infarction were randomly divided into 3 groups: model group (M), low-dose group (L) of total saponins of panax ginseng fruit, high-dose group (H) of total saponins of panax ginseng fruit, 10 in each group. The sham group (S) 10. The intragastric administration is started the next day after the operation, the intragastric administration is carried out on the low-dose group by 19.5mg/kg/d of the ginseng fruit total saponin, the intragastric administration is carried out on the high-dose group by 39mg/kg/d of the ginseng fruit total saponin (the ginseng fruit total saponin is powder in a vibration source capsule), and the intragastric administration is carried out on the pseudo-operation group and the model group by the normal saline with the same volume. Gavage was continued for 4 weeks and body weight was measured weekly. After 4 weeks, blood was collected from orbital venous plexus after mice were anesthetized with isoflurane, hearts were removed after PBS infusion, and connective tissues were stripped. Part of the protein is fixed in 4% paraformaldehyde, and the rest is temporarily stored in liquid nitrogen, and then transferred to-80 ℃ for storage, so as to be used for detecting protein and gene.
1.3 echocardiography testing
Cardiac ultrasound measurements were performed on the mice 2 and 4 weeks after AMI using a Vevo 2100 high resolution imaging system, and Left Ventricular Ejection Fraction (LVEF) and Left ventricular short axis shortening (LVFS) were calculated according to the formulas. LVEF = (left ventricular end diastolic volume-left ventricular end systolic volume)/left ventricular end diastolic volume × 100%, LVFS = (left ventricular end diastolic inner diameter-left ventricular end systolic inner diameter)/left ventricular end diastolic inner diameter × 100%. Cardiac function was assessed.
1.4 serological assays
After the mice were anesthetized with isoflurane, blood was collected from orbital venous plexus and allowed to stand at room temperature for 20min. Centrifuging at 4 deg.C at 3000 rpm, separating serum, and storing at-80 deg.C. Detecting serum creatine kinase MB (CK-MB) by using an ELISA method to observe the myocardial ischemia condition; serum creatinine (S-Cr) and serum alanine transaminase (ALNASE) were used to observe the liver and kidney function.
1.5 histopathological examination
Observing the arrangement of ischemic myocardial tissues and the infiltration condition of inflammatory cells by hematoxylin-eosin (HE) staining; masson stain (Masson) observed ischemic myocardial fibrosis collagen deposition.
1.6 Western blot detection
Detection of myocardial fibrosis-associated proteins in ischemic myocardium by Western Blot: expression of Collagen I (Collagen I), collagen III (Collagen III) and alpha-Smooth muscle actin (. Alpha. -SMA).
2 data of experiments
2.1 Total saponins of Panax ginseng C.A. Meyer improves cardiac function after acute myocardial infarction
The ultrasonic detection of the heart is carried out on 2 weeks and 4 weeks after the acute myocardial infarction of the mice respectively. Compared with the Sham group, the Model group LVEF and LVFS are obviously reduced (P is less than 0.01) in both detection results, which indicates that the modeling of the acute myocardial infarction Model is successful. Compared with the Model group, the LVEF and LVFS of the patient are obviously increased (P is less than 0.01) after the treatment of low and high doses of the total saponins of the ginseng fruits, but the statistical difference (P is more than 0.05) is not generated between the low and high concentration of the saponins of the ginseng fruits (tables 1A-1B and figures 1A-1B), which indicates that the total saponins of the ginseng fruits can obviously improve the cardiac dysfunction induced by acute myocardial infarction.
TABLE 1A 2 week cardiac ultrasonography results of AMIA postoperative in each group of mice: (
n＝8)
Note: in comparison to the Sham group, * p is less than 0.01; in comparison with the Model set, # P＜0.01。
(in Table 1A, model group is represented by M, sham group is represented by S, low dose group is represented by L, and high dose group is represented by H.)
TABLE 1B ultrasonic examination of 4 weeks post-acute myocardial infarction heart of each group of mice (
n＝8)
Note: in comparison to the Sham group, * p is less than 0.01; in comparison with the Model set, # P＜0.01。
2.2 Total saponins of herba Herminii can relieve myocardial injury after acute myocardial infarction, and no toxic and adverse side effects of liver and kidney
The results of the measurement of the serum myocardial damage marker CK-MB, and the liver and kidney function markers ALT and S-cr of each group of mice are shown in Table 2 and FIG. 2. Compared with the Sham group, the serum CK-MB level of the Model group is obviously increased (P is less than 0.01), which indicates that myocardial damage still exists after 4 weeks of acute myocardial infarction. After the low-concentration and high-concentration ginseng fruit total saponins are subjected to dry prediction, the CK-MB level is obviously reduced (P is less than 0.05), and the low-concentration and high-concentration ginseng fruit total saponins have no obvious difference (P is more than 0.05), which indicates that the ginseng fruit total saponins can reduce myocardial damage caused by ischemia. The ALT content in serum has no statistical difference (P is more than 0.05) between groups, which indicates that the total saponins of the ginseng fruit have no hepatotoxicity at the dose of 39mg/kg/d. Compared with the Sham group, the serum S-cr level of the Model group is obviously increased (P is less than 0.05), which indicates that myocardial infarction causes renal function injury, and the low and high dose of the total ginsenoside group has no statistical difference (P is more than 0.05) compared with the Model group, which indicates that the total ginsenoside has no renal toxicity at the dose of 39mg/kg/d.
TABLE 2 CK-MB, ALT and S-cr expression levels (. + -. S, n = 6) in each group of mice
Note: p < 0.01 compared to Sham group; in comparison with the Sham group, § p is less than 0.05; in comparison with the Model set, # p is less than 0.01; in comparison with the Model set, & P＜0.05。
2.3 Total saponins of Panax Ginseng fruit for improving histopathological changes of heart after myocardial infarction
Pathological changes in myocardial tissue following acute myocardial infarction were assessed using HE staining and the results are shown in figure 3. The Sham group has normal myocardial tissue structure, regular muscle fiber trend, clear texture, plump cytoplasm and uniform and consistent myofilament gaps. The Model group has disordered myocardial structure, thick myofilaments, waveform change, unclear texture and infiltration of a large number of inflammatory cells. The change of the myocardial histopathology of the low and high dose ginseng fruit total saponin group is obviously improved.
The degree of myocardial fibrosis after acute myocardial infarction was assessed using Masson staining and the results are shown in figure 4. After Masson staining, collagen fibers appear blue and muscle fibers appear red. A large amount of collagen fiber deposition exists in the myocardial tissue of the Model group, and the collagen deposition is obviously reduced after the ginseng fruit total saponin is given. The volume fraction (CVF) of Collagen is measured by Image J software, and the results show that the CVF of the Model group is obviously increased (P is less than 0.01) and the CVF of the ginsenoside Re dry pre-group is obviously reduced (P is less than 0.05) compared with the Model group compared with the Sham group (figure 5), which indicates that the total saponins of ginseng fruit can improve the myocardial tissue pathological damage induced by acute myocardial infarction.
2.4 expression of fibrosis-associated protein after acute myocardial infarction inhibited by general ginsenoside
Cardiac Fibroblasts (CFs) are the main effector cells of myocardial fibrosis, and under the stimulation of pathological conditions (such as ischemia, pressure overload and inflammation), CFs are activated to transdifferentiate into myofibroblasts with secretion and contraction functions. Activated myofibroblasts are capable of secreting large amounts of extracellular matrix proteins and can regulate matrix remodeling by producing proteases and their inhibitors. alpha-SMA is a specific protein for differentiation of CFs into myofibroblasts. Myocardial fibrosis is mainly caused by the diffuse accumulation of Collagen i and Collagen iii in the interstitium, and thus the degree of myocardial fibrosis can be estimated by measuring their content. The expression conditions of the myocardium alpha-SMA, collagen I and Collagen III are detected by using a Western blot method, and the result is shown in figure 6. Compared with the Sham group, the Model group has obviously increased alpha-SMA expression (P is less than 0.01), which indicates that myocardial ischemia activates myofibroblasts; after the low-dose and high-dose of the total saponins of panax ginseng are subjected to dry prediction, the expression of alpha-SMA is remarkably reduced (P is less than 0.01), and the two groups of the total saponins of panax ginseng have no statistical difference (P is more than 0.05), which indicates that the total saponins of panax ginseng can inhibit the activation of myofibroblasts induced by ischemia. Similarly, acute myocardial infarction results in the overexpression of Collagen I and Collagen III in myocardial tissues, and the total saponins of the ginseng fruits can obviously inhibit the tendency, and the two groups of the total saponins of the ginseng fruits have no statistical difference (P is more than 0.05).
The inventive concept is explained in detail herein using specific examples, which are only provided to help understanding the core idea of the present invention. It should be understood that any obvious modifications, equivalents and other improvements made by those skilled in the art without departing from the spirit of the present invention are included in the scope of the present invention.
Claims (9)
1. Application of herba Herminii total saponin in preparing medicine for resisting myocardial fibrosis is provided.
2. The use of claim 1, wherein the myocardial fibrosis comprises acute myocardial infarction-induced myocardial histopathological injury.
3. The use according to claim 2, wherein the acute myocardial infarction-induced myocardial histopathological injury comprises myocardial collagen fibre deposition following an acute myocardial infarction.
4. The method of claim 1, wherein said anti-myocardial fibrosis comprises decreased expression of myocardial α -SMA, collagen i and Collagen iii.
5. The use of claim 1, wherein the animal dose of the total saponins of panax ginseng fruit is 19.5mg/kg/d to 39mg/kg/d.
6. The use of claim 5, wherein the animal dose of total saponins of panax ginseng is a high dose of 39 mg/kg/day or a low dose of 19.5 mg/kg/day.
7. The medicine for resisting myocardial fibrosis is characterized by comprising effective treatment amount of ginseng fruit total saponin and pharmaceutical auxiliary materials.
8. The anti-myocardial fibrosis medicament of claim 7, wherein the animal administration amount of the total saponins of panax ginseng is 19.5-39 mg/kg/d.
9. The anti-myocardial fibrosis drug of claim 8, wherein the animal administration amount of the total saponins of panax ginseng is 39mg/kg/d at the high dose or 19.5mg/kg/d at the low dose.
Priority Applications (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN202210921892.3A CN115317528A (en) | 2022-08-02 | 2022-08-02 | Application of ginseng fruit total saponin and medicine for resisting myocardial fibrosis |
Applications Claiming Priority (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN202210921892.3A CN115317528A (en) | 2022-08-02 | 2022-08-02 | Application of ginseng fruit total saponin and medicine for resisting myocardial fibrosis |
Publications (1)
| Publication Number | Publication Date |
|---|---|
| CN115317528A true CN115317528A (en) | 2022-11-11 |
Family
ID=83918686
Family Applications (1)
| Application Number | Title | Priority Date | Filing Date |
|---|---|---|---|
| CN202210921892.3A Pending CN115317528A (en) | 2022-08-02 | 2022-08-02 | Application of ginseng fruit total saponin and medicine for resisting myocardial fibrosis |
Country Status (1)
| Country | Link |
|---|---|
| CN (1) | CN115317528A (en) |
Citations (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN110559328A (en) * | 2019-11-01 | 2019-12-13 | 吉林省集安益盛药业股份有限公司 | A method for preparing total saponins of herba Herminii with 11 ginsenosides as fingerprint characteristic components |
-
2022
- 2022-08-02 CN CN202210921892.3A patent/CN115317528A/en active Pending
Patent Citations (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN110559328A (en) * | 2019-11-01 | 2019-12-13 | 吉林省集安益盛药业股份有限公司 | A method for preparing total saponins of herba Herminii with 11 ginsenosides as fingerprint characteristic components |
Non-Patent Citations (4)
| Title |
|---|
| MEIYAN LIU，等: "Antidepressant-like effects of ginseng fruit saponin in myocardial infarction mice" * |
| MEIYAN LIU，等: "Antidepressant-like effects of ginseng fruit saponin in myocardial infarction mice", BIOMEDICINE & PHARMACOTHERAPY, vol. 115, pages 1 * |
| 何小溪，等: "人参果皂苷对大鼠心肌缺血再灌损伤后心室重构的影响", pages 34 * |
| 高洁，等: "振源胶囊的心血管保护作用及临床应用的研究进展", vol. 26, no. 05, pages 991 - 996 * |
Similar Documents
| Publication | Publication Date | Title |
|---|---|---|
| CN114588205B (en) | Application of Tongxinluo in preparing medicine for treating heart failure with preserved ejection fraction | |
| RU2727142C2 (en) | Bisamide derivative of dicarboxylic acid as agent stimulating tissue regeneration and restoration of reduced functions of tissues | |
| CN111840112B (en) | Application of carnosic acid or derivatives thereof in preparing medicine for treating diabetic complications | |
| CN116406265A (en) | Ester group-containing aromatic propionamide compound and application of metabolite thereof in preparation of drugs for treating heart failure | |
| CN113304149A (en) | Application of compound in preparation of medicine for treating type 2 diabetic cardiomyopathy | |
| CN115317528A (en) | Application of ginseng fruit total saponin and medicine for resisting myocardial fibrosis | |
| CN108815171B (en) | Application of 25-hydroxycholesterol in preparation of medicine for treating or preventing myocardial infarction | |
| CN103735550B (en) | A kind of pharmaceutical composition and application thereof for the treatment of chronic kidney disease myocardial damage | |
| CN111067911A (en) | Medical application of pulsatilla saponin B4 in resisting acute gouty arthritis | |
| CN114588212A (en) | New use of traditional Chinese medicine water lettuce for resisting heart failure | |
| CN103417907A (en) | Applications of traditional Chinese medicine composition in preparation of drug used for inhibiting angiogenesis | |
| CN104873482B (en) | A kind of pharmaceutical composition of anti-chronic heart failure | |
| CN105687208B (en) | Application of cycloastragenol in preparation of medicine for treating heart failure | |
| CN104398503B (en) | Use of fargesin and its derivative in preparation of drugs for treating or preventing pulmonary hypertension | |
| CN103622985B (en) | The effect of amarogentin treatment pulmonary hypertension and application thereof | |
| CN112891361B (en) | Application of Pubescenoside C in preparation of medicine for preventing and treating myocardial ischemia-reperfusion injury | |
| WO2023092983A1 (en) | Application of traditional chinese medicine composition in preparation of drugs for treating heart aging | |
| CN102526195A (en) | Medicinal composition for treating coronary disease and preparation method thereof | |
| CN117159549A (en) | Application of ester compound | |
| TWI694835B (en) | Use of short peptide to treat/prevent hypertension and related diseases | |
| CN118319921A (en) | Preparation of medicine for treating cardiomyopathy | |
| CN101987200B (en) | Compound medicine containing antihypertensive peptide and aldosterone receptor antagonist for curing hypertension | |
| CN114306292A (en) | Application of gnelitol in preparing medicine for treating osteoporosis bone defect | |
| Fang et al. | Zhen-wu-tang protects against myocardial fibrosis by inhibiting M1 macrophage polarization via the TLR4/NF-κB pathway | |
| CN110974836A (en) | Application of cyclovirobuxine D in diabetic cardiomyopathy based on Nrf2 |
Legal Events
| Date | Code | Title | Description |
|---|---|---|---|
| PB01 | Publication | ||
| PB01 | Publication | ||
| SE01 | Entry into force of request for substantive examination | ||
| SE01 | Entry into force of request for substantive examination | ||
| RJ01 | Rejection of invention patent application after publication |
Application publication date: 20221111 |
|
| RJ01 | Rejection of invention patent application after publication |