Objective:To establish a model of alcoholic hepatitis in rats and to explore the effect of captopril in the prevention and treatment of alcoholic hepatitis and its anti-inflammatory mechanism. Methods:A total of 127 rats were randomly divided into normal group and modeling group. The modeling group was given intragastric administration of gradient alcohol

and the normal group was given an equal volume of normal saline. After six weeks of modeling

the rats in the modeling group were randomly divided into model group

high-

medium-

and low-dose captopril groups

and silybin positive control group

and continued to be given intragastric administration of alcohol.The rats in the captopril groups and silybin positive control group received respective drugs at a dose determined by equivalent dose calculation based on adult’s and rat’s body surface areas

and those in the normal and model groups were given isovolumetric normal saline. After 6 weeks of administration

blood samples were collected from all rats to measure the levels of alanine aminotransferase（ALT）

aspartate aminotransferase（AST）

high-density lipoprotein cholesterol（HDL-C）

and low-density lipoprotein cholesterol（LDL-C）; the liver was collected to analyze its pathological changes

while the liver tissue homogenate was extracted to measure the levels of nuclear factor-kappa B（NF-κB）and tumor necrosis factor-alpha（TNF-α）. Results:The model group had increased levels of ALT

AST

LDL-C

NF-κB

and TNF-α and a decreased level of HDL-C; the high-dose captopril group had decreased levels of ALT

AST

LDL-C

NF-κB

and TNF-α and an increased level of HDL-C. Liver examination showed that rats in the normal group had normal hepatocyte morphology; rats in the model group had edematous and disorganized hepatocytes

accompanied by inflammatory cell infiltration and necrotic lesions; rats in the high-dose captopril group had obvious alleviation of both hepatocyte edema and inflammatory cell infiltration. Conclusion:Captopril can alleviate alcoholic hepatitis in rats by reducing NF-κB and TNF-α.