Establishment Of Alcoholic Liver Disease Model And Preliminary Research On Reversible Process In Rats

Aim: Alcohol is an important etiological factor of human liver disease. Spontaneousrecovery of alcoholic liver disease in some patients was found in clinic afterabstinence, however, the mechanism and pathological change were not fullyunderstood. We established the rat model of alcoholic liver disease to investigate thepathological changes, serological index and mesenchymal cells apoptosis inspontaneous recovery in alcoholic liver diseases.Methods: 50 SD rats were randomly divided into 5 groups, 10 rats each group (A, B,C, D groups were experimental groups, E was control group). Experimental groupswere fed with high-fat and low-protein diet and given with alcohol intragastricadministration for 12 weeks, then fed with normal rat diet. Control group was givennormal rat diet. A, B, C, D, E groups were killed respectively in first day, 7th day,21th day and 42th day in recovery period, then blood and liver tissue were collected.The pathological changes of alcoholic liver disease were investigated by HE staining,Masson staining andα-SMA immunohistochemistry. The serum levels of ALT, TG,TCH and HDL were determined by colorimetry. CCl4 rat model was established bysubcutaneous injection of CCl4 and compared with alcohol model.Results: The rat model of alcoholic liver disease with the pathological change ofhepatic cell degeneration, necrosis, inflammation and fibrosis was established byusing ethanol, high-fat and low protein diet. During recovery of alcoholic liver disease,hepatic cells ballooning degeneration and necrosis, inflammation were reduced afterHE staining, which had significant differences in 7th day (P＜0.05). The hepaticfibrosis degrees were also decreased gradually and had statistical significance in 21thday (P＜0.05) by using Masson staining, the number ofα-SMA positive cells alsodecreased. These indicated that hepatic cells ballooning degeneration, inflammation,hepatic cells necrosis, deposition of collagen fibrils and number ofα-SMA positivecells showed a reduction in the recovery process. ALT levels of A, B, C, D and Egroups were 61.11±16.84, 48.04±9.23, 40.00±10.11, 38.00±8.61 and 35.33±1.62respectively, and had statistical significance in 7th day (P＜0.05). The levels of TG,TCH and HDL hadn't statistical significance in recovery process (P＞0.05). Inaddition, the increase trend of mesenchymal cells apoptosis was observed, but stillneed to investigate. Extensive fibrosis deposition and pseudo-liver-lobular accompanied withsteatosis, inflammation and necrosis were observed in CCl4 rat model. Steatosis,inflammation and necrosis were reduced in recovery process. Collagen fibrils of CCl4animal model were decreased but every period were more serious than alcohol model.ConclusiConclusion: (1) Rat model of alcoholic liver disease is established successfully usedalcohol, high-fat and low-protein diet, which pathological changes show hepatic cellsdegeneration, necrosis, inflammation, hepatic fibrosis. (2) In the recovery periods,pathological changes of alcoholic liver disease are reversible process in the model. (3)Mesenchymal cells apoptosis may be relevant to the recovery process of alcoholicliver disease.