CN105250247A - Application of astaxanthin in preparation of drugs controlling nonalcohalic fatty liver disease drugs - Google Patents
Application of astaxanthin in preparation of drugs controlling nonalcohalic fatty liver disease drugs Download PDFInfo
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Abstract
The invention discloses application of astaxanthin in preparation of pharmaceutical compositions promoting Nrf-2, HMOX-1 and SOD-1 expression in control of nonalcohalic fatty liver, and discloses a pharmaceutical composition for controlling nonalcohalic fatty liver diseases. And the pharmaceutical composition is characterized by containing astaxanthin.
Description
Technical field
The present invention relates to the application of astaxanthin in preparation control non-alcohol fatty liver medicine, more particularly, the present invention relates to astaxanthin and preparing the application in the medicine suppressing to promote Nrf-2, HMOX-1, SOD-1 to express in non-alcoholic fatty liver.
Background technology
Liver is vitals of glycolipid metabolism, and numerous research in recent years shows, disorders of lipid metabolism plays an important role in type 2 diabetes mellitus develops.When hepatocyte is impaired or function generation obstacle time, hepatocyte synthetic fat albumen reduces, and causes lipoprotein to transport lipid material and transport occurs is obstructed, finally cause athero and occur serious disorders of lipid metabolism.Have investigation display, type 2 diabetes mellitus patient great majority all suffer from fatty liver, and in chronic hepatopathy especially in the patient of fatty liver, the sickness rate of type 2 diabetes mellitus obviously increases and fasting glucose is higher, and both sides relation is close, reciprocal causation.Clinically, for the simultaneous situation of both diseases, treatment is made overall plans often, will take into account treatment chronic hepatic diseases, improve liver function and be then obviously conducive to glycemic control when reducing blood glucose.
The initial main pathology of diabetes liver injury shows as hepatocyte fat lesion, and liver fat lesion also can progressively develop into non-alcoholic stellato-hepatitis, hepatic fibrosis, liver cirrhosis etc., and this is referred to as non-alcohol fatty liver (NAFLD).NAFLD is the important behaviour of metabolism syndrome at liver, and the sickness rate of NAFLD in the whole world is 20%-30%, is also the major reason of various chronic hepatopathy.The generation development of non-alcohol fatty liver can be explained by the hypothesis of " two-hit " or " multiple-strike "." first strike " is insulin resistant and lipodystrophy, hyperinsulinemia is there is during insulin resistant, hyperinsulinemia can promote that liver fat is synthesized, increase free fatty secretion, reduce free-fat acid oxidase, and reduce very low density lipoprotein (VLDL) generation, finally cause the formation of fatty liver." second strike " is on the basis of fatty liver, and hepatocyte damages the even fibrosis that is inflamed further.A series of independent factor such as proinflammatory factor, Adipocyte Factor, mitochondria dysfunction, oxidative stress and the lipid peroxidation factor can inspire " second strike ".Insulin resistant and obesity can increase the gathering of liver tg and promote liver lipogenesis to have report to point out, insulin resistant is considered to one of important factor of non-alcohol fatty liver, but its concrete pathophysiological mechanism is explained not yet completely and illustrates.
Liver is one of first target organs of insulin action, under normal condition, fat metabolic process remains dynamic equilibrium in liver, and when there is disorders of lipid metabolism, hepatocyte pours in a large amount of fat, cause fatty acid to increase in liver, and the final liver lipids that occurs deposit and fatty liver.Many pro-inflammatory chemokine and cytokine such as monocyte chemoattractant protein (MCP-1), tumor necrosis factor (TNF-α), interleukin (IL)-1, interleukin (IL)-6 have also played certain effect in the pathogenesis of non-alcohol fatty liver, studies have reported that TNF-α, IL-1, IL-6 can destroy insulin signaling pathway, promote the generation of insulin resistant and glucose-lipid metabolism disorder, thus weight fat hepatopathy.
The disorders of lipid metabolism that oxidative stress is correlated with is the focus of recently research, has research display, high fat diet can cause lipid peroxidation stress generation and weaken the anti-oxidation function of liver, finally cause liver fat lesion.Lipidosis and response to oxidative stress are most important two factors in causing non-alcohol fatty liver to develop.Treatment at present for fatty liver disease is based on to its pathogenetic understanding, mainly loses weight to improve insulin resistant, and reduces the generation of lipid concentration and minimizing oxidative stress and inflammation.So active prevention and treatment disorders of lipid metabolism become the important step of diabetes and prevention and treatment of complication thereof, for once the glycolipid found is abnormal, except carrying out necessary life style and regulating, also need to do the treatment of further chemoprophylaxis.
Nowadays the whole world all research and development good effect and also toxic and side effects little, the natural lipotropism metabolism disorder medicine even had no side effect, since the beginning of the sixties in last century, the living marine resources with huge potentiality to be exploited are the focuses that the world of medicine pays close attention to always, find the important goal that new living marine resources have now become researches on natural drugs.Astaxanthin (astaxanthin, ASX) full name is 3,3 '-dihydroxy-bata-carotene-4,4 '-one, is a kind of Red carotenoids, is extensively distributed in marine bacteria, algae, in shell-fish and Fish, many bibliographical information astaxanthins have been had to infect at antioxidation, anti-inflammatory, anticancer, anti-helicobacter pylori (HP) and demonstrate powerful effect in uvioresistant lamp process, and rare toxic and side effects.
Increasing result of study shows: astaxanthin, at protection islet beta cell function, improves insulin resistant and prevents and treats diabetes aspect and have suitable medical value.The people such as ZhangM adopt carbon tetrachloride to set up Liver Fibrosis Model, use 20 respectively, 40,80mg/kg dosage carries out astaxanthin treatment to rat, laboratory observation obviously can alleviate the pathological change of hepatic fibrosis to astaxanthin, also can suppress the expression of NF-kb and TGF-β, thus reduces the activation of hepatic stellate cell and the generation of extracellular matrix, especially use heavy dose of astaxanthin intervention, it is larger that hepatic fibrosis improves degree.BhuvaneswariS finds that the non-oxidizability of astaxanthin and antiinflammatory action effectively can reduce the generation of hepatocyte endoplasmic reticulum oxidative stress, stops and delays the chronic sympton that inflammation causes.
The NAFLD cause of disease is complicated, and development and insulin resistant occur for it, fat metabolic disturbance, fat, oxidative stress and closely related, but the molecular mechanism that development occurs for relation between it and NAFELD is still unclear.Clinically, first preventing and correct metabolism disorder of blood lipid, is to the primary prevention of diabetes or early treatment has positive effect.
Summary of the invention
In prior art, also do not have medicine for promoting that Nrf-2, HMOX-1, SOD-1 express in suppression non-alcoholic fatty liver, Nrf-2 refers to nuclear factor E2 correlation factor herein, and HMOX-1 is DELTA rHO-1, and SOD-1 is superoxide dismutase-1.The present inventor sets up and classical feeds by high fat the disorders of lipid metabolism animal model caused, observe astaxanthin feeds rat blood sugar and blood fat impact on high fat, and astaxanthin to this rat liver steatosis and dysfunction whether make moderate progress effect time, surprisingly find that astaxanthin can promote the expression of Nrf-2, HMOX-1, SOD-1 when suppressing non-alcoholic fatty liver, thus complete the present invention.
Intrahepatic fat is deposited in the pathogenesis of insulin resistant and lipids metabolic disturbance in diabetes mellitus and plays pivotal role, type 2 diabetes mellitus patient often increases with free fatty and triglyceride isoconcentration, research display free fatty is had can directly to promote liver lipids to synthesize and glyconeogenesis increase, induced insulin is resisted, and lipid peroxidation can increase the weight of liver fat change, produce non-alcoholic stellato-hepatitis, even hepatic fibrosis.So early intervention fatty liver, to prevention and therapy type 2 diabetes mellitus and complication thereof, there is important clinical meaning.
There is report to point out that astaxanthin can cross over the nuclear membrane of cell membrane, mitochondrial membrane and destination organization, and stablize the structure of these films, reduce or prevent the over oxidation of lipid.The people such as MayumiIkeuchi observe the impact of astaxanthin on the obesity mice of high fat diet, even if found that and give high fat diet, astaxanthin also can suppress the increase of body weight and suppress the increase of fat, in addition, astaxanthin decreases the weight of liver, and serum triglycerides and total cholesterol concentration also significantly reduce.After this research experiment carries out High fat diet to rat before onset diabetes, find that non-intervention group rat carbohydrate tolerance decreases, there is a large amount of fat aggregations and occur large-area fat vacuole pathological changes in liver, serum HDL levels obviously declines, and serum TG and TC concentration obviously increase.With astaxanthin prevention intervention after 4 weeks, find that the carbohydrate tolerance of the more non-intervention group rat of intervention group rat raises to some extent, liver fat vacuole area and quantity all reduce, serum HDL concentration obviously raises, TG and TCH concentration obviously reduces, illustrate that astaxanthin obviously can improve the blood lipid level of carbohydrate tolerance and rat, improve disorders of lipid metabolism.
Research shows that high fat diet is the key factor causing oxidative stress.And another major reason that liver fat becomes is the peroxidating obstacle of lipid, the oxidation of the synthesis and fatty acid that often also affect lipoprotein when lipid peroxidation increases utilizes, thus causes lipogenesis to increase and be piled up in hepatocyte causing fatty liver.Nuclear factor (Nrf-2) signal path is one of significant process of cellular anti-oxidant reaction, wide expression in liver.Nrf-2 is the important transcription factor maintaining cellular redox balance, and have the effect of anti-oxidation stress, under high smectic state, Nrf-2 expression obviously declines, and SOD-1 and HMOX-1 is also significantly suppressed.Nrf-2 can the expression of upregulation downstream target gene superoxide dismutase SOD-1 and Heme oxygenase HMOX-1, and defence oxidation thus Cell protection are from damage.The people such as YueYang feed into non-alcoholic stellato-hepatitis disease model to the first high fat of diabetic mice, with the astaxanthin of various dose, intervention is carried out 12 weeks to mice, found that mice serum glutamate pyruvate transaminase and glutamic oxaloacetic transaminase, GOT concentration, and inflammatory factor concentration significantly declines, the Nrf-2 of one of endogenous anti-oxidative system composition and the expression of down-regulated gene thereof also reduce, and intervene dosage and are directly proportional to therapeutic effect.There is item to study equally as study subject, type 2 diabetes mellitus patient is found that astaxanthin can effective anti-lipid peroxidation marker representation level, significantly reduce oxidative stress.This laboratory observation is to not only before onset diabetes during Primary preventive intervention; the expression of rat liver Nrf-2 and downstream gene SOD-1 and HMOX-1 thereof increases; prompting astaxanthin can significantly suppress the peroxidating of lipid stress; improve the anti-oxidation function of liver; the liver protecting from damage, and then also prevents developing of liver fat lesion.
Astaxanthin (astaxanthin) involved in the present invention, has another name called astaxanthin, Astaxanthin, is a Carotenoids, and be also the highest level product of carotenogenesis, in rediance, chemical constitution is similar to beta-carotene.And beta-carotene, phylloxanthin, canthaxanthin, lycopene etc. are all the intermediate products of carotenogenesis, therefore at nature, astaxanthin has the strongest non-oxidizability.Extensively be present in biosphere, in the feather of particularly shrimp, Eriocheir sinensis, fish, frond, yeast and birds, content is higher, is one of carotenoid main in marine organism.
Astaxanthin chemical name: 3,3 '-dihydroxy-4,4 '-diketo beta-carotene, pigment Aj067-69CASNo:472-61-7, molecular formula C40H52O4, molecular weight is 596.86.Due to hydroxyl (-OH) the optical activity reason at two ends, astaxanthin has 3S-3 ' S, 3R-3 ' S, these 3 kinds of isomery kenels of 3R-3 ' R (also referred to as left-handed, meso, dextrorotation), wherein synthetic astaxanthin is that the mixture of 3 kinds of structure astaxanthins (left-handedly accounts for 25%, dextrorotation accounts for 25%, meso about 50%), few antioxidant activity, completely different with the astaxanthin (based on transconfiguration---3S-3S type) in the aquaculture organism body such as salmon. the astaxanthin in yeast source is 100% dextrorotation (3R-3 ' R), has Partial Antioxidation active; Above-mentioned two kinds of source astaxanthins be mainly used in non-edible animal and goods and materials painted on.Only have the astaxanthin in algae source to be 100% left-handed (3S-3 ' S) structure, there is the strongest biologic activity.
Accompanying drawing explanation
Fig. 1: the experiment flow figure of the embodiment of the present invention 1.
Fig. 2: each group liver tissues of rats Nrf-2, HMOX-1, SOD-1 protein expression band analysis chart in the embodiment of the present invention 1.
Fig. 3: in the embodiment of the present invention 1, (E group and B group compare, * P < 0.05 for the change of each group rat liver Nrf-2 expressing quantity; D group and C group compare, * P < 0.05).
Fig. 4: in the embodiment of the present invention 1 in the embodiment of the present invention 1 change of each group rat liver HMOX-1 expressing quantity (E group and B group compare, * P < 0.05; D group and C group compare, * P < 0.05).
Fig. 5: in the embodiment of the present invention 1, (E group and B group compare, * P < 0.05 for the change of each group rat liver SOD-1 expression; D group and C group compare, * P < 0.05).
Detailed description of the invention
Materials and methods
1.1 laboratory animal
Healthy male Sprague-Dawley (SD) rat, in one month age of Mus, body weight 100-120g, is provided by Zhejiang Province's Experimental Animal Center.Animal sub-cage rearing, laboratory animal starts experiment again after animal center conforms one week, and free drinking water standard rat feed is fed, and keep clean in cage, room temperature controls at 24 DEG C, lamp, well-ventilated, and relative humidity is 60%.Zoopery completes in University Of Ningbo's Experimental Animal Center.
1.2 experimental apparatus and reagent
1.2.1 major experimental instrument
Table 1 experimental apparatus title and manufacturer
1.2.2 experimental drug and reagent
Table 2 experimental drug title and manufacturer
Experimental technique
1.2.32 the successful standard of patients with type Ⅰ DM premorbid state model
Experimental rat first feed with high lipid food (in every 100g, each component ratio is for crude protein: fat: carbohydrate=20: 40: 40) 6 weeks, carry out modeling, cut tail and get blood survey random blood sugar, to guarantee that experimental rat is in state before onset diabetes, observe the mental status of rat every day, ensure sufficient food and drinking-water.
1.2.4 pharmaceutical intervention
Prevention group administration time is 4 weeks and 6 weeks, and given low is 25mg/kg, and all the other groups synchronously give the normal saline of equivalent, free diet drinking-water.
1.2.5 random blood sugar measures and oral glucose tolerance test
In chemoprophylaxis processing procedure, each group every rat surveyed a random blood sugar every 3 days at synchronization, gets hematometry, at once carry out relative recording by automatic blood glucose meter from rat tail vein, added up blood glucose value change after experiment terminates.
In zoopery is carried out, each group rat is respectively at pharmaceutical intervention 4 weeks rear row oral glucose tolerance tests.Concrete grammar is: after Rat Fast 12h, carries out gavage (given low is 2g/kg) with the solution of 50% glucose.After gavage 0h, 0.5h, 1h and 2h, cut tail get tail vein survey blood glucose value.Experiment terminates rear drafting each group of rat glucose tolerance curve, and area under calculating glucose tolerance curve.
1.2.6 blood collection, specimen are fixed and are dyeed with paraffin section, H & E
1.2.6.1 blood sample collection
Blood collection: after treatment terminates, every rat selects angular vein to get blood, and concrete grammar is: get vacuum test tube ready in advance and carry out labelling, and left hand fixes rat, the glass capillary of right hand diameter 1mm about length 5cm is rotatably inserted into inside rat eye, adjust degree of depth posterior vein blood to flow out immediately, access blood with blood taking tube, leave standstill after 2-3h until blood, with the centrifugal 2000rpm of low speed centrifuge, 10min, gets supernatant, detects blood lipids index with automatic biochemical instrument.
1.2.7Westernblot the expression of methods analyst liver Antioxidative Factors Nrf2, HMOX-1, SOD-1 albumen
Table 3Westernblot operating process
[embodiment]
Astaxanthin is to the premorbid Primary preventive intervention effect of type 2 diabetes mellitus
Experiment flow figure in embodiment 1 that Fig. 1 is real.Specifically, 20 healthy male SD rats are divided into five experimental grouies at random, are respectively: A group (Normal group), B group (simple high fat group), and ((high fat+astaxanthin prevention group), often organizes each 4 rats to C group.Normal group is fed with normal rats feedstuff 10 weeks, and all the other are respectively organized rat and all synchronously feed with high lipid food, and from the 7th week, C group rat prevented with the dosage astaxanthin of 25mg/kg, while A, B group give the normal saline of equivalent, the time cycle is 4 weeks.Row OGTT tests afterwards.Each group of rat glucose tolerance curve is described to show the change of rat glucose tolerance after testing and terminating, calculate and area value (AUC) under respectively organizing rat glucose tolerance curve, finally put to death rat and collect serum and tissue samples, detect each group of rat blood serum biochemical indicator subsequently and carry out H & E and dye, observe each group of morphologic change of liver tissues of rats, and detect the change of liver Antioxidative Factors expression by Westernblot method.
Experiment shows, in high fat situation, the expression of liver Nrf-2, HMOX-1, SOD-1 is significantly suppressed.In the present invention, whether hepatic antioxidative function is promoted by Nrf-2 and downstream signal factor HMOX-1 thereof and SOD-1 for understanding astaxanthin, and then the generation suppressing liver fat to become, to protect hepatocyte, this experiment have detected each group of rat liver Nrf-2, HMOX-1, SOD-1 expressing quantity, statistical result shows, as shown in Figure 3-Figure 5, after intervening with astaxanthin, E group (high fat+prevention group) significantly raises (* P < 0.05) than the expression of B group (simple high fat group) Nrf-2, HMOX-1, SOD-1; Meanwhile, compared to C group (high fat+STZ group), the expression of Nrf-2, HMOX-1, SOD-1 of D group (high fat+prevention+STZ group) also significantly increases (* P < 0.05).
Intrahepatic fat is deposited in the pathogenesis of insulin resistant and lipids metabolic disturbance in diabetes mellitus and plays pivotal role, type 2 diabetes mellitus patient often increases with free fatty and triglyceride isoconcentration, research display FFA is had can directly to promote liver lipids to synthesize and glyconeogenesis increase, induced insulin is resisted, and lipid peroxidation can increase the weight of liver fat change, produce non-alcoholic stellato-hepatitis, even hepatic fibrosis.So early intervention fatty liver, to prevention and therapy type 2 diabetes mellitus and complication thereof, there is important clinical meaning.
There is report to point out that astaxanthin can cross over the nuclear membrane of cell membrane, mitochondrial membrane and destination organization, and stablize the structure of these films, reduce or prevent the over oxidation of lipid.The people such as MayumiIkeuchi observe the impact of astaxanthin on the obesity mice of high fat diet, even if found that and give increase that high fat diet astaxanthin also can suppress body weight and the increase suppressing fat, in addition, astaxanthin decreases the weight of liver, and serum triglycerides and total cholesterol concentration also significantly reduce.This research experiment is after prediabetes carries out High fat diet to rat, find that non-intervention group rat carbohydrate tolerance decreases, there is a large amount of fat aggregations and occur large-area fat vacuole pathological changes in liver, serum HDL levels obviously declines, and serum TG and TC concentration obviously increase.With astaxanthin prevention intervention after 4 weeks, find that the carbohydrate tolerance of the more non-intervention group rat of intervention group rat raises to some extent, liver fat vacuole area and quantity all reduce, serum HDL concentration obviously raises, TG and TCH concentration obviously reduces, illustrate that astaxanthin obviously can improve the blood lipid level of carbohydrate tolerance and rat, improve disorders of lipid metabolism.
In the preventive effect experiment in early stage, after the rat that high fat is fed is intervened with astaxanthin, the Histomorphological of liver has good performance, illustrates that astaxanthin has restitution to a certain degree to liver fat lesion, prevents developing of fatty liver.Research shows that high fat diet is the key factor causing oxidative stress.And another major reason that liver fat becomes is the peroxidating obstacle of lipid, the oxidation of the synthesis and fatty acid that often also affect lipoprotein when lipid peroxidation increases utilizes, thus causes lipogenesis to increase and be piled up in hepatocyte causing fatty liver.Nuclear factor (Nrf-2) signal path is one of significant process of cellular anti-oxidant reaction, wide expression in liver.Nrf-2 is the important transcription factor maintaining cellular redox balance, and have the effect of anti-oxidation stress, under high smectic state, Nrf-2 expression obviously declines, and SOD-1 and HMOX-1 is also significantly suppressed.Nrf-2 can the expression of upregulation downstream target gene superoxide dismutase SOD-1 and Heme oxygenase HMOX-1, and defence oxidation thus Cell protection are from damage.The people such as YueYang feed into non-alcoholic stellato-hepatitis disease model to the first high fat of diabetic mice, with the astaxanthin of various dose, intervention is carried out 12 weeks to mice, found that mice serum glutamate pyruvate transaminase and glutamic oxaloacetic transaminase, GOT concentration, and inflammatory factor concentration significantly declines, the Nrf-2 of one of endogenous anti-oxidative system composition and the expression of down-regulated gene thereof also reduce, and intervene dosage and are directly proportional to therapeutic effect.There is item to study equally as study subject, type 2 diabetes mellitus patient is found that astaxanthin can effective anti-lipid peroxidation marker representation level, significantly reduce oxidative stress.This laboratory observation is between prediabetes intervention period, and the expression of rat liver Nrf-2 and downstream gene SOD-1 and HMOX-1 thereof increases.Large quantity research finds, the opposing of high fat diet energy induced insulin occurs, and oxidative stress has played key effect wherein.The a large amount of fat stores of liver can cause T-CHOL, acyl coenzyme A and DG to generate increasing, thus suppresses insulin signaling pathway to cause insulin resistant.The people such as Arunkumar treat type 2 diabetes mellitus animal model rat with astaxanthin, laboratory observation to: the HFFD rat insulin sensitivity after astaxanthin is treated obviously raises, and the serine phosphorylation of IRS (IRS-1 and IRS-2) obviously reduces, facilitate the conduction of insulin signaling pathway, improve insulin resistant thus played and fall hypoglycemic effect.
The research acting on disorders of lipid metabolism in the fat Mus fed at high fat about astaxanthin is at present more, also astaxanthin can cross over cell membrane because of the special molecular structure of self to have research to confirm, but whether it directly acts on Hepatocyte Insulin signal path or still unclear by playing a role between other signaling molecules.In this experiment, the high fat diet in early stage causes liver fat lesion and anti-oxidation stress miopragia, and carbohydrate tolerance declines to some extent, after astaxanthin prevention is intervened, Rats adiposis hepatica alleviates, carbohydrate tolerance these results of recovery obtained to a certain extent all show that astaxanthin passes through to suppress liver fat lesion in preventing diabetes, to play important function, for the relation understanding pathogenesis of diabetes mellitus, diabetes and fatty liver further provides experimental basis.
Table 4 description Chinese and English initialism synopsis
| STZ | Streptozotocin |
| AUC | Area under glucose tolerance curve |
| OGTT | Oral glucose tolerance test |
| HE | Hematoxylin eosin stain |
| Nrf-2 | Nuclear factor E2 correlation factor |
| HMOX-1 | DELTA rHO-1 |
| SOD-1 | Superoxide dismutase-1 |
Claims (10)
1. astaxanthin suppresses the application in the pharmaceutical composition promoting Nrf-2, HMOX-1, SOD-1 to express in non-alcohol fatty liver in preparation.
2. apply as claimed in claim 1, wherein, described astaxanthin is natural astaxanthin.
3. apply as claimed in claim 1 or 2, wherein, described non-alcohol fatty liver is selected from one or more in hepatitis, hepatic fibrosis, liver cirrhosis.
4. apply as claimed in claim 1 or 2, wherein, described non-alcohol fatty liver can cause type 2 diabetes mellitus.
5. apply as claimed in claim 1 or 2, wherein, described non-alcohol fatty liver is from type 2 diabetes mellitus rat diabetes premorbid.
6. prevent a pharmaceutical composition for non-alcohol fatty liver, it is characterized in that, containing astaxanthin.
7. pharmaceutical composition as claimed in claim 7, wherein, described astaxanthin is natural astaxanthin.
8. as claimed in claims 6 or 7 to go compositions, wherein, described non-alcohol fatty liver is selected from one or more in hepatitis, hepatic fibrosis, liver cirrhosis.
9. as claimed in claims 6 or 7 to go compositions, wherein, described non-alcohol fatty liver can cause type 2 diabetes mellitus.
10. as claimed in claims 6 or 7 to go compositions, wherein, described non-alcohol fatty liver is from type 2 diabetes mellitus rat premorbid.
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Cited By (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN115737615A (en) * | 2022-11-28 | 2023-03-07 | 合肥工业大学 | Application of astaxanthin combined positive medicine in preparation of medicine for improving cholestatic liver disease |
| US11696593B2 (en) | 2018-08-24 | 2023-07-11 | Bioscience Formulators, LLC | Astaxanthin nutritional compositions and uses |
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Cited By (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US11696593B2 (en) | 2018-08-24 | 2023-07-11 | Bioscience Formulators, LLC | Astaxanthin nutritional compositions and uses |
| CN115737615A (en) * | 2022-11-28 | 2023-03-07 | 合肥工业大学 | Application of astaxanthin combined positive medicine in preparation of medicine for improving cholestatic liver disease |
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Application publication date: 20160120 |