黄芪甲苷对乙型病毒性肝炎大鼠模型免疫炎症反应的影响及机制

Effect and mechanism of astragaloside Ⅳ on immune inflammatory response in rat model of viral hepatitis B

目的 探讨黄芪甲苷对乙型病毒性肝炎大鼠免疫炎症反应的抑制作用及其作用机制。方法 将SPF级SD大鼠30只随机分为空白对照组、模型组、黄芪甲苷(40 mg/kg)组,每组10只。采用尾静脉注射乙型肝炎病毒的方法制备乙型病毒性肝炎大鼠模型。ELISA试剂盒检测大鼠血清中HBsAg、HBeAg水平;全自动生化分析仪测定血清中丙氨酸转氨酶(Alanine aminotransferase,ALT)、天冬氨酸转氨酶(Aspartate aminotransferase,AST)水平;流式细胞仪检测外周血液中Th17、Treg细胞比例;ELISA检测大鼠血清中IL-1β、IL-6及TNF-α水平;HE染色观察肝组织病理形态。Western blot检测AMPK、NF-κB及IκB蛋白表达。结果 黄芪甲苷能够显著降低大鼠血清HBsAg、HBeAg、ALT及AST水平;明显降低Th17比例,明显升高Treg比例及Treg/Th17;明显降低IL-1β、IL-6及TNF-α水平;明显减轻肝组织损伤;明显增加AMPK与IκB蛋白表达,并明显降低NF-κB蛋白表达。结论 黄芪甲苷可改善乙型病毒性肝炎大鼠免疫炎症反应,保护其肝功能,作用机制可能与调控AMPK/NF-κB信号通路有关。

Objective To investigate the inhibitory effect of astragaloside IV on immune inflammatory response in rats with viral hepatitis B and its mechanism. Methods Thirty SPF SD rats were randomly divided into control group,model group, and astragaloside Ⅳ(40 mg/kg) group, with 10 rats in each group. A rat model of hepatitis B virus was prepared by injecting hepatitis B virus into the tail vein. The levels of HBsAg and HBeAg in rat serum were detected by ELISA. The levels of alanine aminotransferase(ALT) and aspartate aminotransferase(AST) in serum was detected by automatic biochemical analyzer. The proportion of Th17 and Treg cells in peripheral blood was detected by flow cytometry. The levels of IL-1β, IL-6 and TNF-α in rat serum were detected by ELISA. The pathological morphology of liver tissue was observed by HE staining. The expression of AMPK, NF-κB and IκB were detected by Western blot. Results Astragaloside IV could significantly reduced the levels of HBsAg, HBeAg, ALT and AST in serum, significantly reduced the Th17 ratio,significantly increased the Treg ratio and Treg/Th17, significantly reduced the levels of IL-1β, IL-6 and TNF-α,significantly reduced liver tissue damage, significantly increased the expression of AMPK and IκB, and significantly reduced the expression of NF-κB. Conclusion Astragaloside Ⅳ can improve immune inflammatory response and protect the liver function of viral hepatitis B rats, and the mechanism may be related to the regulation of AMPK/NF-κB signaling pathway.