Objective:Based on the PI3K/Akt/m TOR signaling pathway and autophagy to explore the mechanism of Rougan Jiangmei Decoction against rats liver fibrosis.Methods:The rat liver fibrosis model was prepared by intraperitoneal injection of 40%olive oil CCl4mixed solution with 3 m L·kg-1.The experiment was divided into control group,model group,Rougan Jiangmei Decoction low dose group,Rougan Jiangmei Decoction high dose group and colchicine group,with 10rats in each group.The rat liver pathology was observed by HE and Masson staining.The serum levels of ALT and AST were measured by using ALT,AST kit.The serum levels of TNF-αand IL-6 by using Elisa.The expression level ofα-SMA in liver tissues detected by immunohistochemistry.And the protein expression levels of PI3K,p-PI3K,Akt,p-Akt,m TOR,p-m TOR,P62,Beclin-1,LC3-I,LC3-II,α-SMA,Col-1 in rats detected by Western Blot.Results:Compared with the control group,model group rats liver sinuses narrowed,inflammatory cells severely infiltrated,liver lobules unclear,false leaflets appear,with lipid droplet vacuoles,blue-stained fibers increased.Serum levels of ALT,AST,TNF-α,and IL-6 were significantly increased in model group rats(P<0.01).The expression ofα-SMA,Col-1,Beclin-1,and LC3-II protein was significantly increased in the liver tissues of the model group rats(P<0.01).The protein expression of P62,p-PI3K,p-Akt,and p-m TOR were significantly decreased(P<0.05,P<0.01).Compared with the model group,Rougan Jiangmei low and high group rats liver lobe structure was intact,inflammatory infiltration improved.Serum ALT,AST,TNF-α,and IL-6 were significantly decreased in Rougan Jiangmei low and high group rats(P<0.01).The expression ofα-SMA,Col-1,Beclin-1,LC3-II protein were significantly decreased in the liver tissues of the Rougan Jiangmei low and high group rats(P<0.01).The protein expression of P62,p-PI3K,p-Akt,p-m TOR were significantly increased(P<0.05,P<0.01).Conclusion:The mechanism of Rougan Jiangmei Decoction anti-rats liver fibrosis may be related to enhance PI3K/Akt/m TOR signaling pathway and inhibit of autophagy. |