加味茵芍散对非酒精性脂肪性肝病大鼠干预作用及机制探讨

Discussion on mechanism and intervention effects of Jiawei Yinshao Powder on NAFLD rats

目的:探讨加味茵芍散对非酒精性脂肪性肝病(NAFLD)大鼠的防治作用及其机制。方法:采用高脂乳剂灌胃建立大鼠NAFLD模型,分别给予多烯磷脂酰胆碱及加味茵芍散中药灌胃干预,计算和检测各组大鼠肝指数、胰岛素抵抗指数(HOMA-IR)、NF-κB、TNF-αm RNA的表达水平并观察肝组织病理学改变。结果:与模型组比较,中药各剂量组大鼠血清TC、TG、LDL-C、FFA、FPG、AST、ALT、FINS、HOMA-IR水平、肝指数及肝脏MDA水平显著降低(P<0.05),血清HDL-C及肝脏SOD、T-GSH结果显著升高(P<0.05),肝脏病理切片显示加味茵芍散可明显减轻肝细胞脂肪变性及炎性反应细胞浸润等病理症状。Real-time PCR结果示,给予高剂量加味茵芍散的大鼠肝脏组织内NF-κB、TNF-α在m RNA水平上均低于模型组和胆碱组大鼠(P<0.05)。结论:加味茵芍散能够有效减轻NAFLD大鼠肝脏脂肪变性,对NAFLD具有较好的防治功效。其作用机制可能与抑制或下调NF-κB、TNF-αm RNA表达,从而阻断IKKβ/NF-κB细胞通路的激活有关。

Objective： To discuss mechanism and intervention effects of Jiawei Yinshao Powder on nonalcoholic fatty liver disease （NAFLD） rats. Methods： The NAFLD rats model was modeled by intragastric administration of high-fat emulsion, and the rats were respectively intervened with intragastric administration of polyene phosphatidyl choline and Jiawei Yinshao Powder. Liver index, insulin resistance index （HOMA-IR）, the mRNA levels of NF-κB and TNF-α in each group were calculated and detected, and the histopathological changes of liver tissue were observed. Results： Compared with the model group, the levels of these were significantly decreased in Jiawei Yinshao Powder group, such as the levels of TC, TG, LDL-C, FFA, FPG, AST, ALT, FINS and HOMA-IR in serum, the liver index and the MDA level in liver （P〈0.05）. The serum HDL-C and SOD, T-GSH in liver significantly increased （P〈0.05）. The pathological section of liver showed that Jiawei Yinshao Powder could significantly decreased the hepatic steatosis and inflammatory cell infiltration. The Real-time PCR results showed mRNA levels of NF-κB and TNF- α in liver tissues of rats given Jiawei Yinshao Powder high dose were both lower than those in the model group and the choline group（P〈0,05）. Conclusion： Jiawei Yinshao Powder can effectively reduce hepatic steatosis in rats with NAFLD and have better effect on NAFLD. Its mechanism of effects may be related to inhibiting or down-regulating the expression of NF-κB and TNF- α mRNA level, then blocking the activation of IKK β/NF-κB signaling pathway.