| Objective:By setting up rat models of alcoholic liver disease, to observe the pathology and ultramicro-stucture changes in the process of alcoholic liver disease development, and to investigate the variations of leptin expression and liver function, also to investigate the oxidation and anti-oxidation index. And treating with low molecular weight heparin, thus to reveal the mechanism of alcoholic liver disease and to provide experiment basis for clinical therapy.Methods:Forty-five male Sprague-Dawley rats weighting between160g and200g were fed for one week. Then divided into two groups randomizedly:model group and control group, thirty rats in the model group and fifteen rats in the control group. The model group rats were given alcoholic intragastric administration by56%alcohol. The alcohol was administrated chronically twice a day in the first two weeks,56%alcohol was infused by2g/kg,3g/kg,4g/kg,5g/kg,6g/kg,7g/kg,8g/kg in turn every two days. And then the model group rats were given intragastric administration with56%alcohol8g/kg until the10week to produce the alcoholic liver disease model. The control group rats were given intragastric administration with physiological saline. We extracted two rats from the model group to observe the pathology change. If there were fat drops diffuseing in the liver tissue, we initially established an alcoholic liver disease. Then the model group rats were divided into low molecular weight heparin treatment group and alcoholic liver disease group randomizedly. Both the two groups continued to be given alcoholic intragastric administration, and the low molecular weight heparin treatment group was received100IU/kg low molecular weight heparin hypodermic injection. And the control group also were divided into normal control group and low molecular weight heparin control group randomizedly. All the groups were treated for four weeks. Then they were killed by laparotomy after anesthesia. Respectively determinated the hepatic function parameters, serum leptin. Weighted the body weight, liver weight and liver index (liver weight/body weight). And determinated the MDA,SOD,GSH-PX in serum and liver tissue with spectrophotometry. Liver histological pathology was dyed by haematoxylin-eosin staining under light microscope and the ultramicro-structure were observed under electron microscope.Results:Compared with control groups, in the alcoholic liver disease group, the hepatic function such as ALT,AST,ALP,TG,TC,LDL and leptin increased significantly (P <0.05), the MDA content in the serum and liver tissue rised, and the enzymatic activity of SOD,GSH-PX decreased (P<0.05); The trestment group got lighter than the alcoholic liver disease group (P<0.05); There were no significant between normal control group and low molecular weight heparin (P>0.05). In the alcoholic liver disease group, many small drops of lipids infiltration were seen throughout the liver tissue after twelve weeks, and partly displayed alcoholic hepatitis manifestation. The severity of liver tissue ultramicro-structure changes associated with the hepatic function and pathology manifestation. We could find that many lipid drops appeared in the alcoholic liver disease group and the mitochondrial membrane was destroyed; while the severity of low molecular heparin treatment group weakened.Conclusions:1. We copied the alcoholic liver disease rats model by alcohol intragastric in fourteen weeks.2. The increase of the level of leptin and lipid peroxidation were related with alcoholic liver disease.3. Low molecular weight heparin has an excellent therapeutic effect on alcoholic liver disease by reducing lipids deposits, inhibiting chronic inflammation and fibrosis. We inferred that low molecular weight heparin may improve fat metabolism, inhibit oxidatie stress and reduce leptin expression.4.There was no side effect on normal rats, ruling out the drug itself for the development of alcoholic liver disease. |
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