OBJECTIVE: To explore the role of Kupffer cells in non-alcoholic steatohepatitis (NASH) by means of rat model. METHODS: Nineteen male SD rats were randomized into model group (n=10) and normal group (n=9), with a high-fat diet and standard diet for 12 weeks, respectively. Routine histologic features of hepatic section were observed by HE staining. The number and shape of Kupffer cells in the liver were detected by immunohistochemistry and penetrated electron microscope, respectively. RESULTS: All rats of model group developed NASH, which was characterized by obesity and hyperlipidemia. Histopathological examination showed hepatocellular macrovesicular steatosis, lobular inflammatory cell infiltration and necrosis. Compared with normal group, the count of Kupffer cells in the liver was largely increased, and the Kupffer cells in the model group were activated to some extent. Furthermore, these changes of Kupffer cells were in accordance with the degree of steatosis, inflammation and necrosis in the liver of the model group. CONCLUSION: The number and activity of Kupffer cells are increased significantly in NASH induced by high-fat diet, and Kupffer cells might be involved in the pathogenesis of steatohepatitis.
OBJECTIVE: To explore the role of Kupffer cells in non-alcoholic steatohepatitis (NASH) by means of rat model. METHODS: Nineteen male SD rats were randomized into model group (n=10) and normal group (n=9), with a high-fat diet and standard diet for 12 weeks, respectively. Routine histologic features of hepatic section were observed by HE staining. The number and shape of Kupffer cells in the liver were detected by immunohistochemistry and penetrated electron microscope, respectively. RESULTS: All rats of model group developed NASH, which was characterized by obesity and hyperlipidemia. Histopathological examination showed hepatocellular macrovesicular steatosis, lobular inflammatory cell infiltration and necrosis. Compared with normal group, the count of Kupffer cells in the liver was largely increased, and the Kupffer cells in the model group were activated to some extent. Furthermore, these changes of Kupffer cells were in accordance with the degree of steatosis, inflammation and necrosis in the liver of the model group. CONCLUSION: The number and activity of Kupffer cells are increased significantly in NASH induced by high-fat diet, and Kupffer cells might be involved in the pathogenesis of steatohepatitis.