CN101066272A - Application of compound 6-furfuryl amino purine in preparing medicine for treating myocardial tissue oxidizing damage - Google Patents
Application of compound 6-furfuryl amino purine in preparing medicine for treating myocardial tissue oxidizing damage Download PDFInfo
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- CN101066272A CN101066272A CN 200710017984 CN200710017984A CN101066272A CN 101066272 A CN101066272 A CN 101066272A CN 200710017984 CN200710017984 CN 200710017984 CN 200710017984 A CN200710017984 A CN 200710017984A CN 101066272 A CN101066272 A CN 101066272A
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Abstract
The present invention discloses application of compound 6-furfuryl amino purine in preparing medicine for treating myocardial tissue oxidizing damage. Compound 6-furfuryl amino purine as one kind of exogenic purine matter can raise the antioxidase SOD, CAT and GSH-Px activity of myocardial tissue, capture and eliminate free radical directly, prevent or suppress the damage of oxygen free radical reaction and lipoid preoxidation on myocardial cell membrane, myocardial mitochondrion and intracellular biomacromolecule, and raise myocardial ability in resisting oxidation damage, so as to maintain the integrity of myocardial cell structure and function and maintain the myocardial normal physiological function.
Description
Technical field
The present invention relates to the new pharmaceutical uses of chemical compound 6-bran amidopurin (6-Furfurylaminopurine), be particularly related to the application that chemical compound 6-bran amidopurin is used to prepare treatment myocardial tissue oxidizing damage medicine, experimentation according to the applicant proves, chemical compound 6-bran amidopurin can improve the oxidation resistance of animal body under the oxidative damage state, can be used in preparation treatment myocardial tissue oxidizing damage medicine.
Background technology
Heart is body " kinetic pump ", and it promotes blood flow, provides ample amount of blood flow to organ, tissue, with supply oxygen and various nutrient substance, and takes away metabolic end-product, makes other organs, histiocyte keep normal metabolism and function.Various endocrine hormones and some humoral factors also will be transported to target cell by blood circulation in the body, realize that the body fluid of body is regulated, and keep the constant relatively of organismic internal environment.In addition, the realization of blood defence function, and the constant relatively adjusting of body temperature also all will rely on blood and constantly circulate in blood vessel, and circulating of blood are because the effect of heart " pump " realizes.
The physiological function of heart " pump " is shunk by myocardial cell and is finished, myocardial cell is rich in mitochondrion, mitochondrion is the main source of free radical, all contain a large amount of unsaturated fatty acids in mitochondrial duplicature and the cell membrane, these characteristics of cardiac muscular tissue have determined it to be easy to be subjected to the damage of lipid peroxidation.Studies show that, the lipid peroxidation that radical damage cardiac muscular tissue is brought out can participate in myocardiac generation: activities of antioxidant enzymes reduces in the cardiomyopathy patient body, radical scavenging activity is descended, free radical generates and increases in a large number, lipid peroxidation strengthens, destroy the membranous structure and the interior biomacromolecule of cell of myocardial cell, cause the reduction of cardiac contractility ability, thereby quicken the process of disease.Therefore, the integrity that keeps the myocardial cell 26S Proteasome Structure and Function is carried out its normal physiological function to myocardial cell contractile function and heart great important.
The accumulation of oxidative damage is the main cause that causes animal body aging and disease.The toxicity of oxygen is not because the respond of oxygen molecule itself, but, comprise superoxide anion, hydrogen peroxide molecule, hydroxy radical, hydroperoxy, hydroperoxides, alkoxyl, alkane peroxy and singlet oxygen because oxygen molecule is reduced into the many intermediate products that produce in the water process.These intermediate products comprise free radical and molecule, are referred to as active oxygen, but custom calls free radical to them.Reactive oxygen free radical is mainly derived from xanthine oxidase system and mitochondrion in the body, and xanthine oxidase is present in the body with the xanthine dehydrogenase form usually, and its catalytic reaction does not form free radical.But when ATP exhaustion or oxidative stress, xanthine dehydrogenase is converted into xanthine oxidase, and the xanthine oxidase that catalysis ATP metabolism produces changes into uric acid and generates O
2 -, O
2 -Reactive poor in aqueous medium, disperse is fast, and very fast dismutation by enzyme is converted into O
2, generate OH through reduction reaction
-Mitochondrial respiratory chain under normal circumstances only produces a small amount of oxygen-derived free radicals, causes a large amount of oxygen-derived free radicals to generate when mitochondrial function is impaired, and body is caused more serious damage.
Under normal circumstances, the generation of oxygen-derived free radicals and removing are in dynamic equilibrium in the cardiac muscular tissue, have the complete antioxidase system of a cover to protect cardiac muscle not to be subjected to the oxidative damage of free radical in the animal body.But under the situation of morbid state and aging, because the reduction of activities of antioxidant enzymes in the cardiac muscular tissue, unnecessary oxygen-derived free radicals can not be by timely, effectively removing, make myocardial cell be subjected to oxidative damage, especially lipid peroxidation will cause the Radical Metabolism disorder and produce a large amount of free radicals the damage of mitochondrion double membrane structure, the latter is the injury of myocardium tissue further, influences its normal physiological function.
Therefore, myocardial tissue oxidizing damage is the very common and serious damage that animal and human's body is faced, and can cause the aging of animal and human's body and the generation of other diseases, increases the weight of the aging and the pathological changes of body.At present, the medicine of anti-myocardium oxidative damage is few on the market, and is difficult for extracting acquisition, exists purity not high, and effective ingredient is indeterminate, and shortcomings such as price height have been brought very big trouble to application.Therefore, it is wide to develop a kind of source, the purity height, and definite ingredients, effective, very urgent of the medicine of the anti-myocardium oxidative damage that safety non-toxic is harmless and being significant.
6-furfuryl group amidopurin is that Mliller in 1956 finds in the herring sperm dna extract that heat sterilization is crossed a kind ofly has an active micromolecular compound of the cell division of promotion.It is a kind of non-natural basic element of cell division, be commonly called as kinetins (kinetin, KT), molecular formula C
10H
9N
5O.Pure product are white solid, and fusing point is 265-266 ℃, are amphoteric compound.Be soluble in dilute hydrochloric acid or dilute alkaline soln; Be insoluble in water, ethanol, ether and acetone.The molecular structural formula of its 6-bran amidopurin is as follows:
6-furfuryl group amidopurin is that first is found the material with basic element of cell division effect.In plant, except that having the effect that promotes cell division, differentiation and growth, also has the organ senescence of delaying, the induced bud differentiation increases stomatal aperture, and callus induction sprouts, remove apical dominance, break the lateral bud dormancy and promote germination, delay protein and chlorophyllous Degradation.At present, 6-furfuryl group amidopurin is mainly used in plant tissue culture, and promote cell division and regulate cell differentiation, slow down aging, preserving fruit and vegetable utilizing is regulated the nutrient substance transportation, promotes aspects such as solid.
Antioxidation and the antidotal effect of 6-bran amidopurin aspect plant is very tangible, also do not attempt on animal and human's body.
Summary of the invention
The object of the present invention is to provide 6-bran amidopurin to improve the new purposes of animal and human body-centered flesh oxidation resistance, the applicant finds first that through a large amount of tests 6-bran amidopurin has the effect of anti-oxidative damage to cardiac muscle, proved that 6-bran amidopurin has the anti-oxidative damage effect equally in animal and human's body, can be applicable to improve the exploitation of myocardium anti-oxidative damage ability medicine, also can be applied to the exploitation of antisenescence health product.Can be used for the Application and Development of all dosage forms at present, as powder, pill, tablet, injection, electuary, unguentum, nano-emulsion, capsule or oral liquid etc., administering mode is oral, injection or transdermal administration, and consumption is limited in the 450mg/kgbw.
Description of drawings
Fig. 1 is the influence of 6-bran amidopurin to sarcostyle, Z line and mitochondria ultrastructure in the mouse aging cardiac muscle; Wherein, figure (A) is an I group (TEM * 15,000): Z line, sarcostyle arrangement and mitochondrion are all normal.II organizes (TEM * 15,000): the Z line broadens, blurs; Sarcostyle fracture, dissolving, coagulation; Mitochondrial swelling, vacuolation, ridge disappear.Figure (C) is IV group (TEM * 17,000): the Z line is clear; The sarcostyle marshalling, dissolving, coagulation is slight; Mitochondrial swelling, vacuolation reduce.Figure (D) organizes (TEM * 40,000) for IV: Z line, M line are clear; The sarcostyle marshalling; Typical case's muscle segment structure.
The present invention is further illustrated below in conjunction with concrete test that accompanying drawing and inventor provide.
The specific embodiment
Myocardium oxidative damage of the present invention comprises physiological, pathologic or medicine cardiac muscle oxidative damage.
Described physiological cardiac muscle oxidative damage is the myocardium oxidative damage that body aging damage, strenuous exercise's damage or myocardium long-term load cause.
Described pathologic cardiac muscle oxidative damage is the caused myocardium oxidative damage of disease that the myocardium oxidative damage that causes of the perfusion of myocardial infarction, myocardial ischemia-again or diabetes are followed the free-radical oxidation damage.
Described medicine myocardial damage is directly or indirectly to cause the myocardium oxidative damage that a large amount of chemical drugss that produce of free radical cause by D-galactose, hydrogen peroxide, sodium dithionite, daunorubicin, amycin, goose cream gill fungus toxin or isoproterenol.
Below be the concrete test that the inventor provides, be used to verify that 6-bran amidopurin can be used in the medicinal application that preparation improves myocardium anti-oxidative damage ability.
1 materials and methods
1.1 main agents
6-bran amidopurin: purchase in the Xiamen star is grand and reach the chemical reagent company limited, produce by U.S. Sanland company; Use 0.06molL
-1Hydrochloric acid be mixed with storing solution, 4 ℃ of preservations are standby, use 2molL before the use
-1The NaOH titration is near neutral.D-gal: Chemical Reagent Co., Ltd., Sinopharm Group, lot number is F20050711, normal saline is made into 5gL
-1Solution, 4 ℃ of preservations are standby.SOD detection kit, lot number are 20060322; CAT detection kit, lot number are 20060325; GSH-Px detection kit, lot number are 20060523; MDA detection kit, lot number are 20060320; Coomassie brilliant blue protein detection kit, lot number are 20060323; NO detection kit, lot number are 20060325; All build up bio-engineering research institute available from Nanjing.All the other agents useful for same are analytical pure.
1.2 key instrument
The H-600 transmission electron microscope, HIT; UV 1102 ultraviolet-uisible spectrophotometers, Shanghai Techcomp Instrument Ltd.; BS224S ten thousand/electronic balance, Beijing Sai Duolisi instrument system company limited; HS10268 type 10～100 μ l pipettors: DRAGONMED company produces.
1.3 laboratory animal
A cleaning level ICR mice (Mus muscculus), male, body weight (20.0 ± 2.0) g, available from Xi'an Jiaotong University Medical College's Experimental Animal Center, the quality certification number: Shan moving card word 08-004 number.
1.4 animal grouping and processing
45 mices are divided into 5 groups at random, 9 every group: I group (matched group), II group (aging model group), III group～V organize (6-bran amidopurin protection group).III group～V organizes and irritates stomach 10mgkg every day respectively
-1, 20mgkg
-1, 40mgkg
-16-bran amidopurin, and the nape subcutaneous injection 125mgkg of portion simultaneously
-1D-gal; The II group is irritated the hydrochloric acid of stomach equivalent, the subcutaneous injection 125mgkg of nape portion every day
-1D-gal; The I group is irritated the hydrochloric acid of stomach equivalent, the normal saline of nape portion subcutaneous injection equivalent every day; Handled for 6 weeks continuously, weigh weekly, regulate dosage.
1.56-the bran amidopurin is to the metabolic influence of mouse aging myocardial freedom base
Randomly draw 4 mices in 43d from each group and put to death, it is dirty and in quality to core: the ratio of volume=1: 9 adds 4 ℃ of normal saline and makes 10% tissue homogenate, and the centrifuging and taking supernatant is to be measured.By the requirement of test kit description, measure total protein content with the Coomassie brilliant blue method; Xanthine oxidase is measured the SOD vigor; Ultraviolet spectrometry is measured the CAT activity; Dtnb assay GSH-Px activity; The TBA method is measured MDA content; Chemical determination NO content.
1.66-the bran amidopurin is to the mouse aging myocardial ultrastructure effects
Put to death each group residue mice in 43d, get its cardiac muscular tissue, be cut into about 1mm on ice fast
3Fritter, 4 ℃ of 4% glutaraldehydes are fixing down, ethanol dewaters step by step, electron microscopic section is made in the epoxy resin embedding, the H-600 transmission electron microscope is observed the myocardial cell ultrastructure down.
1.7 data analysis
Date processing uses medical statistics software SPLM 3.0 (Statistical Program for LinearModeling) to carry out variance analysis, and result of the test is with average ± standard deviation (X ± SD) expression.
2 results
2.16-the bran amidopurin is to the metabolic influence of mouse aging myocardial freedom base
Table 16-bran amidopurin is to the metabolic influence of mouse aging myocardial freedom base (n=4, X ± SD)
| Group | SOD Activity (U·mgprot -1) | CAT Activity (U·mgprot -1) | GSH-Px Activity (U·mgprot -1) | NO Level (μmol·l -1) | MDA Level (nmol·mgprot -1) |
| I | 94.049±4.275 | 54.183±2.320 | 32.373±2.850 | 4.572±0.244 | 9.936±0.302 |
| II | 73.439±1.712A | 34.696±4.183A | 20.380±0.852A | 12.159±1.425A | 17.292±2.085A |
| III | 77.799±3.694AC | 42.657±3.272Abd | 23.432±2.259Ac | 9.420±0.733AbC | 14.953±1.066Ac |
| IV | 87.241±3.849aB | 47.313±2.195aBD | 28.038±1.583aB | 6.438±0.637aBD | 11.300±1.529B |
| V | 71.514±1.500AC | 36.047±3.302A | 20.121±1.167AC | 10.715±1.257A | 14.459±1.505Ac |
Annotate: with the expression significant difference (P＜0.05) of marking lower case behind the column data, capitalization is represented difference extremely remarkable (P＜0.01), and a, A represent to compare with the I group, and b, B show with the II group and compare that c, C represent to organize relatively with IV, and d, D represent to organize relatively with V.
As shown in Table 1: compare with I group (blank group), the antioxidase SOD (73.439 ± 1.712 of II group (aging model group) mouse cardiac muscle tissue,-21.9%, P＜0.01), CAT (34.696 ± 4.183,-36.0%, P＜0.01) and GSH-Px (20.380 ± 0.852 ,-37.0%, P＜0.01) activity extremely significantly reduce; MDA (17.292 ± 2.085 ,+74.0%, P＜0.01) and NO (12.159 ± 1.425 ,+165.9%, P＜0.01) content extremely significantly raise, and this shows that the D-galactose can consume antioxidase in the cardiac muscle by upsetting Radical Metabolism; Compare with the II group, in the 6-bran amidopurin protection group, every index all has certain improvement, and is the most obvious with the IV group: SOD:+18.8%, P＜0.01; CAT:+36.4%, P＜0.01; GSH-Px:+37.6%, P＜0.01; MDA:-34.7%, P＜0.01; NO:-47.1%, P＜0.01; Compare SOD, CAT, GSH-Px and NO differences significantly (P＜0.05) with the I group, the MDA there was no significant difference illustrates 20mgkg
-16-bran amidopurin can improve the D-galactose extremely significantly and cause activities of antioxidant enzymes in the mouse aging cardiac muscular tissue, reduce free-radical contents.
2.26-the bran amidopurin is to the mouse aging myocardial ultrastructure effects
By Fig. 1-A as can be known: I group muscle segment is evenly distributed, and respectively is with clearly, and the Z line is clear; The sarcostyle marshalling moves towards consistent, no myofilament fracture distortion; The mitochondrion size is consistent, the ridge queueing discipline, and substrate is even, medium electron density.By Fig. 1-B as can be known: II group Z line increases thick distortion, and the light and shade band is fuzzy; The sarcostyle arrangement disorder, the part fracture, local myofilament disappears; The dissolving of the enlargement of diffusivity mitochondrion, ridge, the fracture of part film, the substrate electron density reduces, and illustrate that the D-galactose causes that cellular metabolism is disorderly and a large amount of radical pair myocardial ultrastructure generation have produced the oxidative damage effect.By Fig. 1-C, 1-D as can be known, compare with model group, Z line, the M line of IV group are clear; The sarcostyle marshalling, dissolving, coagulation reduce; The slight swelling of mitochondrion, vacuolation reduce ridge queueing discipline, the medium electron density of substrate; Visible typical muscle segment structure under the high power lens.20mgkg is described
-16-bran amidopurin can obviously resist the oxidative damage of the radical pair myocardial ultrastructure that the D-galactose causes, the myocardial cell ultrastructure is played a very good protection.
3 conclusions
Experimental result shows, 6-bran amidopurin raises to the active reduction of the inductive mouse aging SOD of cardiac muscular tissue of D-galactose, CAT and GSH-Px and NO and MDA content and has significant inhibitory effect, and it is all extremely remarkable that the every index of 6-bran amidopurin group is compared difference with the aging model group; Transmission electron microscope observing can be kept the myocardial cell normal ultrastructure to 6-bran amidopurin simultaneously, and protection sarcostyle, muscle segment structure and mitochondrion are avoided the oxidative damage of free radical, keeps the integrity of myocardial cell 26S Proteasome Structure and Function.Can prove that by this experiment 6-bran amidopurin has the effect that the raising mouse cardiac muscle is organized the anti-oxidative damage ability.
Claims (8)
1. chemical compound 6-bran amidopurin is used to prepare the application of treatment myocardial tissue oxidizing damage medicine.
2. application as claimed in claim 1 is characterized in that, described myocardium oxidative damage comprises physiological, pathologic or medicine cardiac muscle oxidative damage.
3. application as claimed in claim 2 is characterized in that, described physiological cardiac muscle oxidative damage is the myocardium oxidative damage that body aging damage, strenuous exercise's damage or myocardium long-term load cause.
4. application as claimed in claim 2 is characterized in that, described pathologic cardiac muscle oxidative damage is the caused myocardium oxidative damage of disease that the myocardium oxidative damage that causes of the perfusion of myocardial infarction, myocardial ischemia-again or diabetes are followed the free-radical oxidation damage.
5. application as claimed in claim 2, it is characterized in that described medicine myocardial damage is directly or indirectly to cause the myocardium oxidative damage that a large amount of chemical drugss that produce of free radical cause by D-galactose, hydrogen peroxide, sodium dithionite, daunorubicin, amycin, goose cream gill fungus toxin or isoproterenol.
6. application as claimed in claim 1 is characterized in that, the myocardium oxidative damage medicine of described treatment is cardiac drug, strengthen the motor capacity medicine, delay myocardium old and feeble medicine, protection medicine or strengthen the medicine of myocardium anti-oxidative damage ability before the art.
7. application as claimed in claim 6 is characterized in that, the administering mode of described medicine is oral, injection or transdermal administration, and consumption is limited in the 450mg/kgbw.
8. application as claimed in claim 6 is characterized in that described medicine is made powder, pill, tablet, injection, electuary, unguentum, nano-emulsion, capsule or oral liquid.
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Cited By (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| AU2014214561B2 (en) * | 2013-02-11 | 2018-04-26 | Mitokinin, Inc. | Compositions and methods for treating neurodegenerative diseases |
| US10851109B2 (en) | 2014-02-11 | 2020-12-01 | Mitokinin Llc | Compositions and methods of using the same for treatment of neurodegenerative and mitochondrial disease |
| US11414419B2 (en) | 2017-06-21 | 2022-08-16 | Mitokinin, Inc. | Substituted purines for the treatment of neurodegenerative and mitochondrial diseases |
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2007
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Cited By (7)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| AU2014214561B2 (en) * | 2013-02-11 | 2018-04-26 | Mitokinin, Inc. | Compositions and methods for treating neurodegenerative diseases |
| AU2014214561C1 (en) * | 2013-02-11 | 2019-01-17 | Mitokinin, Inc. | Compositions and methods for treating neurodegenerative diseases |
| AU2018202438B2 (en) * | 2013-02-11 | 2020-01-16 | Mitokinin, Inc. | Compositions and methods for treating neurodegenerative diseases and cardiomyopathy |
| US10723737B2 (en) | 2013-02-11 | 2020-07-28 | The Regents Of The University Of California | Compositions and methods for treating neurodegenerative diseases and cardiomyopathy |
| US11427588B2 (en) | 2013-02-11 | 2022-08-30 | The Regents Of The University Of California | Compositions and methods for treating neurodegenerative diseases and cardiomyopathy |
| US10851109B2 (en) | 2014-02-11 | 2020-12-01 | Mitokinin Llc | Compositions and methods of using the same for treatment of neurodegenerative and mitochondrial disease |
| US11414419B2 (en) | 2017-06-21 | 2022-08-16 | Mitokinin, Inc. | Substituted purines for the treatment of neurodegenerative and mitochondrial diseases |
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