CN113197884A - Application of alpha-ketobutyric acid in preparation of medicine for preventing and/or treating non-alcoholic fatty liver disease - Google Patents
Application of alpha-ketobutyric acid in preparation of medicine for preventing and/or treating non-alcoholic fatty liver disease Download PDFInfo
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Abstract
The invention provides application of alpha-ketobutyric acid in preparing a medicament for preventing and/or treating non-alcoholic fatty liver, belonging to the technical field of liver disease medicaments. Use of alpha-ketobutyrate for the manufacture of a medicament for the treatment of non-alcoholic fatty liver disease. The invention takes a mouse High Fat Diet (HFD) induced non-alcoholic fatty liver disease mouse model as an object, alpha-ketobutyric acid administration treatment is carried out, and results show that the alpha-ketobutyric acid treatment can obviously reduce the weight and the liver weight of a mouse fed with a high fat diet, reduce the liver fat accumulation and the fat cell size of the mouse fed with the high fat diet, reduce insulin resistance of the mouse fed with the high fat diet and reduce liver function damage and blood fat level of the mouse fed with the high fat diet. The alpha-ketobutyric acid improves the relevant symptoms of the non-alcoholic fatty liver mouse, and simultaneously, the alpha-ketobutyric acid is an endogenous compound, has strong pharmacological action and small side effect, thereby providing a basis for clinically treating the non-alcoholic fatty liver.
Description
Technical Field
The invention belongs to the technical field of liver disease drugs, and particularly relates to application of alpha-ketobutyric acid in preparation of a drug for preventing and/or treating non-alcoholic fatty liver.
Background
Non-alcoholic fatty liver disease (NAFLD), a comprehensive clinical disease characterized by hepatocellular steatosis and fat accumulation, includes a series of lesions of simple fatty liver, Non-alcoholic steatohepatitis (NASH), hepatic fibrosis and cirrhosis. Non-alcoholic fatty liver disease is the most common chronic liver disease in the world at present, and has become a worldwide health problem. Despite recent steady progress in defining therapeutic targets and advancing drug development to elucidate the pathogenesis of non-alcoholic fatty liver disease, significant unsolved challenges remain.
Over the past few decades, basic and transformation studies have increased understanding of the pathogenesis of non-alcoholic fatty liver disease and have identified some potential therapeutic targets. Currently, the main treatment means of non-alcoholic fatty liver disease include lifestyle intervention treatment, drug therapy, and the like. In recent years, new technologies such as FXR agonists and fecal transplantation therapies have been applied to NAFLD therapy, and although they have a certain therapeutic effect, these therapies use exogenous components in the body, often face the body's own immune response, have large side effects, and may have obstacles to clinical application.
Disclosure of Invention
In view of the above, the present invention aims to provide an application of an endogenous compound α -ketobutyrate (α -ketobutyrate) in the preparation of a drug for preventing and/or treating non-alcoholic fatty liver disease, which can eliminate autoimmune reaction, has small side effects, and makes it possible to clinically treat novel non-alcoholic fatty liver disease with α -ketobutyrate.
The invention provides application of alpha-ketobutyric acid with a structure shown in a formula I in preparing a medicament for preventing and/or treating non-alcoholic fatty liver;
preferably, the alpha-ketobutyric acid is used for preparing the medicine for treating the non-alcoholic fatty liver by reducing the accumulation of the fat in the liver and the size of fat cells.
Preferably, the alpha-ketobutyric acid treats non-alcoholic fatty liver disease by reducing insulin resistance.
Preferably, the alpha-ketobutyric acid treats non-alcoholic fatty liver by reducing liver function impairment and blood lipid levels.
Preferably, the indicators of impaired liver function include alanine aminotransferases and aspartate aminotransferases.
Preferably, the blood lipid level includes the content of triglycerides and total cholesterol in serum
Preferably, the non-alcoholic fatty liver disease is High Fat Diet (HFD) -induced non-alcoholic fatty liver disease.
Preferably, the dosage form of the medicament comprises an oral dosage form.
Preferably, the dosage of the alpha-ketobutyric acid is not less than 100mg/kg body weight of the mouse.
The invention provides application of alpha-ketobutyric acid with a structure shown in a formula I in preparation of a medicine for preventing and/or treating non-alcoholic fatty liver. Tests have shown that α -ketobutyrate treatment is effective in reducing the weight and liver weight of mice fed a High Fat Diet (HFD); alpha-ketobutyrate treatment reduces liver fat accumulation and adipocyte size in mice fed a High Fat Diet (HFD); alpha-ketobutyrate treatment reduces insulin resistance in mice fed a High Fat Diet (HFD); alpha-ketobutyrate treatment reduced liver function impairment and blood lipid levels in mice fed a High Fat Diet (HFD). Meanwhile, the alpha-ketobutyric acid is an endogenous compound of an organism, has strong pharmacological action and small side effect, and avoids causing anaphylactic reaction, thereby providing a foundation for clinically treating the non-alcoholic fatty liver.
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FIG. 1A is the body weight results of alpha-ketobutyric acid treatment (gavage 100mg/kg) for 4 weeks after a 12-week period of High Fat Diet (HFD);
FIG. 1B is the liver volume results of alpha-ketobutyric acid treatment (gavage 100mg/kg) for 4 weeks after High Fat Diet (HFD) for 12 weeks;
FIG. 2 is the HE and oil red O staining results of liver tissue treated with alpha-ketobutyric acid (gavage 100mg/kg) for 4 weeks after 12 weeks of High Fat Diet (HFD); taking mouse liver tissues for HE and oil red O staining;
FIG. 3 shows the results of staining after a High Fat Diet (HFD) for 12 weeks with alpha-ketobutyric acid treatment (gavage 100mg/kg) for 4 weeks;
FIG. 4A shows the results of glucose measurements after a 12-week period of High Fat Diet (HFD) and 4 weeks of α -ketobutyric treatment (gavage 100 mg/kg);
FIG. 4B shows the results of insulin detection after a 12-week period of High Fat Diet (HFD) for 4 weeks of α -ketobutyric acid treatment (gavage 100 mg/kg);
FIG. 5A shows ALT and AST levels measured after a 12-week period of High Fat Diet (HFD) for 4 weeks after α -ketobutyric acid treatment (gavage 100 mg/kg);
FIG. 5B shows the results of blood lipid measurements after a 12-week period of High Fat Diet (HFD) and 4 weeks of α -ketobutyric treatment (gavage 100 mg/kg).
Detailed Description
The invention provides application of alpha-ketobutyric acid with a structure shown in a formula I in preparing a medicament for preventing and/or treating non-alcoholic fatty liver;
in the present invention, the molecular formula of α -ketobutyric acid is C4H6O3, and the molecular weight of α -ketobutyric acid is 102.09. The source of α -ketobutyric acid in the present invention is not particularly limited, and any source of α -ketobutyric acid known in the art may be used. In the present example, the α -ketobutyric acid is purchased from Shanghai Michelin Biotechnology Ltd under the trade name C12040413.
In the invention, a High Fat Diet (HFD) -induced non-alcoholic fatty liver model is taken as an experimental object, and the non-alcoholic fatty liver model is treated by intragastric administration of alpha-ketobutyric acid for 4 weeks, and the result shows that the alpha-ketobutyric acid achieves the aim of treating the non-alcoholic fatty liver by reducing the weight of a mouse fed with the High Fat Diet (HFD), reducing the weight of liver fat accumulation and the size of fat cells, reducing insulin resistance, and reducing liver function damage and blood fat level. Wherein the indicator of impaired liver function preferably comprises alanine aminotransferase and aspartate aminotransferase. The blood lipid levels preferably include the levels of triglycerides and total cholesterol in the serum. Therefore, the present invention preferably provides the use of α -ketobutyric acid in the treatment of non-alcoholic fatty liver disease.
In the present invention, the dosage form of the drug preferably includes an oral preparation. The type of the oral preparation is not particularly limited in the present invention, and those known in the art, for example, granules, tablets, etc. may be used. The dosage of the alpha-ketobutyric acid is preferably not less than 100mg/kg body weight of the mouse, and more preferably 110-140 mg/kg body weight of the mouse.
The following examples are provided to illustrate the application of α -ketobutyric acid of the present invention in the preparation of drugs for preventing and/or treating non-alcoholic fatty liver, but they should not be construed as limiting the scope of the present invention.
Example 1
Establishment of High Fat Diet (HFD) -induced non-alcoholic fatty liver model
1. Method for feeding mice
Male C57BL/6J mice, 6 weeks old, SPF grade, body mass (20. + -.2) g, purchased from the department of laboratory animals university of Kunming medical sciences (SCXK (Dian) K2020-0004). The mice are 6 mice per cage, and are raised in a light-dark cycle and temperature control environment for 12 hours. The temperature is 26 +/-2 ℃, the relative humidity is 55% +/-5%, and the water is freely eaten and drunk. The experimental animal drinking water is subpackaged with tap water after being autoclaved. All animal experiments of this example were performed as per the animal experimental protocol. Animal ethics committee of university of kunming medical science approved and approved ethics for the animals of this study.
2. Feeding of High Fat Diet (HFD) -induced non-alcoholic fatty liver disease model mice
The establishment of a High Fat Diet (HFD) -induced non-alcoholic fatty liver model was performed with reference to the method described by Tong Zou et al Scientific Reports (2018). The purchased male C57BL/6J mice were acclimatized for one week, and randomly divided into 2 groups of 10 mice each according to body weight, and a Normal Diet (ND) group and a High Fat Diet (HFD) group were set. Wherein the high fat feed is purchased from Beijing Borai Macroda Biotechnology Co., Ltd (HD001, HFD:45 kcal), and the control feed (ND:10 kcal%) is purchased from Australian cooperative feed Co., Ltd. Mice were fed with free-diet drinking water for normal control and high-fat diet. Establishment of a High Fat Diet (HFD) -induced non-alcoholic fatty liver disease mouse model was determined by measuring the body weight of the mouse and oil red O staining of liver tissue, wherein the body weight of the mouse reached 42g and accumulation of oil red O of liver tissue reached 30% of the visual field area indicating successful establishment of the non-alcoholic fatty liver disease mouse model.
Example 2
Methods of treating High Fat Diet (HFD) -induced non-alcoholic fatty liver disease (HFD) mouse models by administering alpha-ketobutyric acid (alpha-kB)
1. Control group and administration group grouping method
The total was divided into a normal group (normal mouse group), a high fat diet group (HFD group), and a dosing group (HFD + α -kB), 3 mice per group, and 3 replicates per group. Wherein, the administration group is started after the mice are modeled for 12 weeks, the alpha-ketobutyric acid is administered according to the standard of 100mg/kg body weight, and the administration is carried out by the intragastric administration once a day for 4 weeks. The normal group and the high fat diet group mice continued to be fed on their respective diets. The body weights of the mice in each group were weighed and recorded every week during the experiment, and the mental status, food intake, etc. of the mice were observed.
The results are shown in FIG. 1A and FIG. 1B. The results showed that the weight and liver weight of the mice in the administered group (HFD + alpha-kB) were significantly reduced compared to the mice in the HFD group.
2. Mouse liver tissue adipose histopathology assay
The mice were sacrificed 4 weeks after the administration of each of the above groups of mice, and liver tissues were isolated. The liver tissue was collected and fixed with a fixative. Liver tissues were examined by HE staining (hematoxylin, eosin staining) and oil red O staining.
The results are shown in FIG. 2. The results showed that the liver of the HFD group mice had significant fat accumulation compared to the normal group (ND) mice. After the prognosis of the alpha-ketobutyric acid, the fat accumulation of the liver tissue of the mouse is obviously reduced compared with that of the HFD group.
The mice were sacrificed 4 weeks after the administration of each of the above groups of mice, and adipose tissues were isolated. The collected adipose tissues were fixed with a fixative. Adipose tissue was examined by HE staining (hematoxylin, eosin staining).
The results are shown in FIG. 3. The staining results showed that the fat cells were significantly increased in HFD group mice compared to normal group (ND) mice. The size of fat cells of mice in an HFD group is obviously reduced after the alpha-ketobutyric acid treatment.
3. Oral glucose tolerance test and insulin tolerance test
Glucose Tolerance Test (OGTT) is carried out on a dosing group and a non-dosing group (a blank group and a high fat diet group) by emptying the fed feed one day ahead (over 12h), measuring the fasting blood glucose value the next day, then intragastrically irrigating 20% glucose solution (2.0g/kg body weight) for experimental animals, and detecting the blood glucose value 15, 30, 60, 90 and 120min after glucose infusion in a timing manner. The difference in the statistical time points of the curves is made.
The blood sugar detection method comprises the steps of inserting the blood sugar test paper into an activating instrument of the Roche glucometer, cutting a gap with the length of about 2mm at the tail tip of the mouse by using a scalpel, extruding a drop of blood to the end of a blood sample groove of the blood sugar test paper, filling the whole blood sample groove with the blood, and displaying the blood sugar value (mmol/L) of the mouse by using a display screen of the instrument.
The results are shown in FIG. 4A. The results show that α -ketobutyrate can improve glucose tolerance (GTT) in HFD mice.
Insulin resistance test (ITT) was performed on the treated and non-treated groups before 4h to empty the feed. Measuring fasting blood glucose, injecting 1U/kg body weight insulin into mouse, and detecting blood glucose at 15, 30, 60, and 90 min. The blood glucose value after insulin injection is divided by the fasting blood glucose value, and a graph is made for comparison.
The insulin detection method is that the prepared serum sample is placed on ice for standby. The kit is stored at 4 ℃, taken out of a refrigerator in advance when in use and balanced to room temperature. Serum insulin was detected by Enzyme-linked immunosorbent assay (ELISA) (mouse insulin Enzyme-linked immunosorbent assay kit) (Yunyan Jiangsu Bi, Cat. No.: PI602) according to the protocol.
The results are shown in FIG. 4B. The results show that alpha-ketobutyric acid can increase insulin sensitivity (ITT) in HFD mice.
4. Serum pathology test
4.1 mice were sacrificed 4 weeks after administration of each of the above groups of mice, blood was collected, and serum was isolated. Serum samples were tested for Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST), indices of liver function impairment.
The detection of alanine aminotransferase was carried out using an alanine aminotransferase assay kit (Rissen Bio Inc., Shandong, cat # 161091) -ALT (IFCC Rate method). The detection principle is that the amino transfer of the L-alanine is catalyzed by ALT to generate the pyruvic acid. Pyruvic acid reacts with NADH under the catalysis of LDH to generate lactic acid and NAD + NADH which have specific absorption peaks at 340nm, the oxidation rate of the lactic acid and the NAD + NADH is in direct proportion to the activity of ALT in serum, and the ALT activity can be measured by measuring the NADH reduction rate at 340 nm.
Detection of aspartate aminotransferase an aspartate aminotransferase assay kit (Shandong Kelison Bio Inc., cat # 161101) (aspartate substrate method) was used; oxaloacetate is produced by AST catalysis of transamination of L-aspartic acid. The latter reacts with NADH under the catalysis of malate dehydrogenase to generate malic acid and NAD + NADH with specific absorption peaks at 340nm, the oxidation rate is in direct proportion to the activity of ALT in serum, and the AST activity can be measured by measuring the NADH reduction rate at 340 nm.
The results are shown in FIG. 5A. The results show that compared with the Normal (ND) mice, the serum ALT and AST levels of the HFD mice are obviously increased, and the serum ALT and AST levels of the mice are obviously reduced after the alpha-ketobutyric acid treatment, which indicates that the liver injury is recovered to a certain extent.
4.2 detecting the content of Triglyceride (TG) and Total Cholesterol (TC) in serum
Triglyceride was detected using a triglyceride measurement kit (GPO-PAP method) (Shandong Kelaisen Bio Inc., cat # 164031). The detection principle is that triglyceride is decomposed by lipase to generate glycerol, the glycerol generates glycerol triphosphate under the action of glycerol kinase, the glycerol triphosphate forms dihydroxyacetone phosphate and hydrogen peroxide under the action of glycerol phosphate oxidase, the latter develops color under the action of peroxidase, and the dye forms maximum absorption at 500nm, and the color intensity is in direct proportion to the content of triglyceride in serum.
Total cholesterol was detected using a total cholesterol assay kit (CHOD-PAP method) (Shandong Kelison Biotech Co., Ltd., cat # 164021). The detection principle is that esterified cholesterol is hydrolyzed by enzyme and oxidized by cholesterol oxidase to generate H2O2Reacting with 4-aminoantipyrine and phenol to generate quinonimine. Quinoneimine has specific absorption at 520nm, and the color generated by the reaction is in direct proportion to the content of cholesterol.
The results are shown in FIG. 5B. The results show that compared with the Normal (ND) mice, the serum Triglyceride (TC) and total cholesterol (TG) contents of the HFD mice are obviously increased, and after the alpha-ketobutyric acid treatment, the serum TG contents of the HFD mice are obviously reduced, and the TC contents are in a descending trend, but the difference is not statistically significant.
The foregoing is only a preferred embodiment of the present invention, and it should be noted that, for those skilled in the art, various modifications and decorations can be made without departing from the principle of the present invention, and these modifications and decorations should also be regarded as the protection scope of the present invention.
Claims (9)
1. The structure is the application of the alpha-ketobutyric acid shown in the formula I in the preparation of the medicine for preventing and/or treating the non-alcoholic fatty liver;
2. the use according to claim 1, wherein said α -ketobutyric acid is used for the preparation of a medicament for the treatment of non-alcoholic fatty liver disease by reducing the accumulation of liver fat and the size of adipocytes.
3. The use of claim 1, wherein said α -ketobutyric acid treats non-alcoholic fatty liver disease by reducing insulin resistance.
4. The use according to claim 1, wherein the α -ketobutyric acid treats non-alcoholic fatty liver disease by reducing liver function impairment and blood lipid levels.
5. The use of claim 4, wherein the indication of impaired liver function comprises alanine aminotransferase and aspartate aminotransferase.
6. The use according to claim 4, wherein the blood lipid levels include the levels of triglycerides and total cholesterol in the serum.
7. The use according to claim 1, wherein the non-alcoholic fatty liver disease is High Fat Diet (HFD) -induced non-alcoholic fatty liver disease.
8. The use of claim 1, wherein the pharmaceutical dosage form comprises an oral dosage form.
9. The use according to any one of claims 1 to 8, wherein the α -ketobutyric acid is administered in an amount of not less than 100mg/kg body weight of the mouse.
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Cited By (1)
| Publication number | Priority date | Publication date | Assignee | Title |
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| CN115074276A (en) * | 2022-06-24 | 2022-09-20 | 无锡特殊食品与营养健康研究院有限公司 | Clostridium pralatanorum capable of relieving non-alcoholic fatty liver and application thereof |
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| CN115074276A (en) * | 2022-06-24 | 2022-09-20 | 无锡特殊食品与营养健康研究院有限公司 | Clostridium pralatanorum capable of relieving non-alcoholic fatty liver and application thereof |
| CN115074276B (en) * | 2022-06-24 | 2024-01-02 | 无锡特殊食品与营养健康研究院有限公司 | Clostridium praecox capable of relieving non-alcoholic fatty liver disease and application thereof |
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