目的：观察芪术颗粒在肝纤维化形成过程中对磷脂酰肌醇-3-激酶/丝氨酸蛋白激酶(PI3K/Akt)信号传导通路的影响,进一步阐明其抗肝纤维化的作用机制。方法将Wistar大鼠随机分为正常组、模型组、实验对照组和芪术颗粒组,采用四氯化碳复制肝纤维化模型,造模同日即给予相应治疗,芪术颗粒组2 g/(kg•d)灌胃,体积为1.0 mL/100 g体质量,实验对照组、模型组给予等体积无菌水,正常组正常喂养。分别于造模后第1、2、4周处理、取材,Western blot免疫印迹法检测p-Akt(Ser473)、p-Akt(Thr308)、Bad(Ser136)、Caspase9蛋白表达。结果与正常组比较,模型组、芪术颗粒组各时间点p-Akt(Ser473)、p-Akt(Thr308)、Bad(Ser136)、Caspase9蛋白表达均升高(P＜0.05)。与模型组比较,第1、2、4周时芪术颗粒组p-Akt(Ser473)表达显著降低,第1、4周Caspase9表达显著降低,差异有统计学意义(P＜0.05,P＜0.01)；p-Akt(Thr308)、Bad(Ser136)表达低于模型组,但差异无统计学意义(P＞0.05)。结论芪术颗粒对PI3K/Akt信号传导通路的激活有调控作用,从而抑制肝纤维化的发生和发展。%Objective To observe the effects of Qishu granule on PI3K/Akt signaling transduction pathways in the process of hepatic fibrosis, and further explain the anti-hepatic fibrosis mechanism of Qishu granule.Methods Wistar rats were randomly divided into normal group, model group, experimental control group and Qishu granule group. Liver fibrosis was duplicated in rats by intraperitoneal injection of CCl4, and the rats were given appropriate treatment at the same day. Rats in Qishu granule group were given a gavage 2 g/(kg•d), 1.0 mL/100 g, while rats in experimental control group and normal group were given the same amount of aquae sterilisata. Rats in each group were taken liver tissue samples in the 1st, 2nd and 4th week, and were checked for the protein expression levels of p-Akt (Ser473), p-Akt (Thr308), Bad (Ser136) and Caspase9 by Western blot.Results Compared with the model group, expression levels of p-Akt (Ser473), p-Akt (Thr308), Bad (Ser136) and Caspase9 in model and Qishu granule groups increased in every time points (P<0.05). Compared with the model group, expression level of p-Akt (Ser473) in Qishu granule group decreased significantly in the 1st, 2nd, and 4th weeks, expression level of Caspase9 dropped in the 1st and the 4th weeks, with statistical significance (P<0.05,P<0.01);expressions of p-Akt (Thr308) and Bad (Ser136) were lower than those in model group, without statistical significance (P>0.05).Conclusion Qishu granule could regulate PI3K/Akt signaling transduction pathways, and inhibit the occurrence and development of liver fibrosis.
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