关键词: 非酒精性脂肪性肝炎, 氧化应激, 血红素氧合酶(HO-1), 丁酸钠

Abstract: Objective To explore the mechanism of heme oxygenase-1(HO-1) in the alleviation of non-alcoholic steatohepatitis (NASH) by sodium butyrate (SB). Methods 1)Mice were randomly divided into a control group, a high-fat high-cholesterol group(HF group) and a high-fat high-cholesterol+natriumbutyrate group (HF+SB group). The total cholesterol (TC), triglycerides(TG), alanine aminotransferase(ALT), aspartate aminotransferase(AST), and tumor necrosis factor(TNF-α) in serum of each group were measured using colorimetric methods. Mice livers were isolated and morphological changes were observed with microscopy by HE and Masson staining. The expression of TNF-α, collagen(COL), and HO-1 in the liver tissues were detected by Western blot; 2)HepG2 cells were divided into a control group, a control+sodium butyrate group (control+SB group), a model group(model group), and a model+sodium butyrate group (model+SB group), and the expression of the aforementioned indicators was measured in each group. Results 1)SB intervention significantly reduced the body weight, liver weight, and liver weight index of NASH mice(P＜0.05),decreased the level of TC, TG, ALT, AST, and TNF-α in serum as well as the expression of TNF-α and collagen(COL) proteins in the liver of NASH mice(P＜0.05). At the same time, SB intervention significantly increased the expression of HO-1 protein in the liver tissue of NASH mice(P＜0.05);2)SB intervention significantly reduced the level of TC, TG, ALT and AST in group model cells and increased HO-1 protein expression in group model cells (all P＜0.05). Conclusions HO-1 plays a crucial role in the alleviation of NASH by sodium butgrate, potentially through mechanisms related to the suppression of hepatic inflammatory and oxidative stress responses.

Key words: non-alcoholic steatohepatitis, oxidative stress, heme oxygenase-1(HO-1), sodium butyrate