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Background: In recent years, long-term, the incidence of heavy drinking of alcoholic liver disease (ALD) in China's ever-increasing, and if left untreated can develop liver fibrosis, cirrhosis and even liver cancer. ALD method in the clinical treatment of major and alcohol, the effect of other medications is less than ideal. Therefore, in addition to Alcoholics ALD early treatment of the current problems to be solved. The currently accepted ALD pathogenesis of excess ethanol in the liver is converted to acetaldehyde, ethanol and acetaldehyde in the tricarboxylic acid cycle disorders and decreased fatty acid oxidation lead to fat deposition in liver cells, and can lead to oxidative stress and lipid peroxidation oxidation. Liver antioxidant system when ALD was destroyed, a serious lack of antioxidants, and therefore a potent treatment antioxidants confrontation ALD oxidative stress and lipid oxidation largely restore normal liver physiological functions. α-lipoic acid (alpha-lipoic acid, LA) is the only known both antioxidants, but also play a role in the lipid phase in the aqueous phase by the action of a variety of ways so that cells from oxidative damage, hailed as a \Studies have shown that The LA has stronger antioxidant activity than VitC, VitE antioxidants and renewable VitC, VitE, glutathione antioxidant. Clinical trials to LA to certain diseases, such as diabetes and liver ischemia-reperfusion injury has a better therapeutic effect, but few studies of the treatment of alcoholic liver disease. Objective: To observe the LA alcoholic liver injury, serum ALT, AST, liver tissue SOD, MDA, GSH-Px, NO, iNOS, CYPIIE1 activity impact explore LA on treatment of alcoholic liver injury in rats. Methods: ethanol feeding rat model. 50 male Wistar rats were randomly divided into five groups. Normal control group (n = 10), model group (n = 10), the treatment group (each group, n = 10), respectively, on the basis of the modeling to give LA100mg / (kg · d), reduced glutathione ( GSH) 600mg / (kg · d), LAl00mg / (kg · d) joint GSH600mg / (kg · d). After 10 days of treatment measurement of serum ALT, AST, liver tissue SOD, MDA, GSH-Px, NO, expression of iNOS, CYPIIE1 content. Results: all treated rats compared with model group each index differences are significant sex (P lt; 0.05), pairwise comparisons between the treatment groups, the LA group and the GSH group SOD CYPIIE1 difference was not statistically significant (P gt; 0.05), the rest of the indicators of differences are significant sex (P lt; 0.05); combined treatment group and the LA group MDA showed no statistical significance (P gt; 0.05), the rest of the indicators of the differences were significant sex (P lt; 0.05 ); combined treatment group and the GSH group indicators differences were significant significant (P lt; 0.05): LA group, the the GSH group with normal group each index difference was statistically significant (P lt; 0.05), the combined treatment group and the normal group MDA difference was not statistically significant (P gt; 0.05), the rest of the indicators of difference is still statistically significant (P lt; 0.05). Pathology observed in treated rats liver steatosis, inflammation and necrosis compared with the model group were mitigate LA group than in the the GSH group improved significantly, the most significant pathological improvement of the combined treatment group. Conclusion: LA can significantly improve the ALD serum biochemical indicators and histopathological changes, ALD has significant therapeutic effects, and more effective than of GSH. The the LA treatment ALD mechanism and its decreased liver MDA content, increase the activity of SOD to inhibit liver tissue the iNOS, CYPIIE1 expression factors. The experiments show that LA with GSH has a synergistic effect in the treatment of ALD, both combination therapy ALD has better efficacy.
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