论文部分内容阅读
本文旨在研究正丁酸钠预处理对刀豆蛋白A(concanavalin A,Con A)诱导的小鼠急性肝损伤的保护作用及机制。给小鼠腹腔注射正丁酸钠(500 mg/kg)0.5 h后,尾静脉注射Con A(15 mg/kg)诱导小鼠急性肝损伤模型,测定小鼠血清谷丙转氨酶(alanine aminotransferase,ALT)、谷草转氨酶(aspartate aminotransferase,AST)的水平;HE染色观察病理学改变;ELISA法检测血清肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、干扰素-γ(interferon-γ,IFN-γ)和高迁移率族蛋白B1(high-mobility group box 1,HMGB1)水平;RT-PCR和免疫组化法检测小鼠肝组织HMBG1的表达与释放。结果显示,正丁酸钠预处理能明显降低Con A诱导的急性肝损伤小鼠血清中ALT和AST水平(P<0.01);显著改善肝组织损伤程度;明显降低血清中TNF-α和IFN-γ的水平(P<0.01);显著抑制肝组织HMGB1的表达与释放(P<0.05或P<0.01)。以上结果提示,正丁酸钠预处理对Con A所诱导的小鼠急性肝损伤具有保护作用,可能与其减少炎性细胞因子TNF-α和IFN-γ的产生及抑制HMGB1的表达与释放有关。
This study aimed to investigate the protective effects of sodium n-butylate (Na-BUTY) on the acute liver injury induced by concanavalin A (Con A) in mice and its mechanism. The mice were injected intraperitoneally with n-butyrate (500 mg / kg) for 0.5 h. After the mice were injected with Con A (15 mg / kg) via the tail vein, acute liver injury model was induced in mice. Alanine aminotransferase ) And aspartate aminotransferase (AST) were measured. The pathological changes were observed by HE staining. The levels of tumor necrosis factor-α (TNF-α), interferon-γ IFN-γ) and high-mobility group box 1 (HMGB1). The expression and release of HMBG1 were detected by RT-PCR and immunohistochemistry. The results showed that n-butyrate preconditioning could significantly reduce the levels of ALT and AST in serum induced by Con A-induced acute liver injury (P <0.01), significantly improve the degree of liver injury, and significantly decrease the levels of TNF-α and IFN- γ (P <0.01), and significantly inhibited the expression and release of HMGB1 in liver tissue (P <0.05 or P <0.01). These results suggest that sodium n-butyrate preconditioning may have a protective effect on Con A-induced acute liver injury in mice, which may be related to the reduction of the production of inflammatory cytokines TNF-α and IFN-γ and the inhibition of HMGB1 expression and release.