ω-3PUFA Inhibit Hepatic Fibrosis by Activating LKB1-AMPK Signal Pathway
ω-3PUFA Inhibit Hepatic Fibrosis by Activating LKB1-AMPK Signal Pathway
Genfei Zhu, Xiaoqing Wu, Xianzhong Qian and Hong Hong*
ABSTRACT
Hepatic stellate cell (HSC) lines were cultured in vitro and treated with different concentrations of Ω-3PUFA. The effects of Ω-3PUFA on the survival rate of HSCs were detected by MTT, and the α-SMA, collagen I, TIMP-1 and MMP-13 proteins were detected by Western blot method. The rat model of hepatic fibrosis was established and divided into control group, model group and omega-3PUFA intervention model group. The effect of Ω-3PUFA on HSC fibrosis was detected by Masson staining, the levels of ALT and AST in serum were detected, and the relative proteins in liver tissue were detected by Western blot. Compared with the group A, 100 mm and 200 mm ω-3PUFA inhibited cell survival in a concentration-dependent manner, while 100 and 200mM ω-3PUFA decreased the expression of α-SMA, collagen Iand TIMP-1 protein in HSCs, while increased the expression level of MMP-13 protein in HSCs. The collagen fiber area of the liver tissue in the group C was reduced than that in the group B. The serum ALT and AST in the group B were raised, while these in the group C were reduced than those in the group A. The p-LKB1 protein in the group B was raised and the p-AMPK was reduced, while the p-LKB1 protein in group C was reduced and the level of p-AMPK was raised compared group A. Omega-3PUFA can significantly inhibit the activation of HSCs and reduce the degree of hepatic fibrosis by regulating LKB1-AMPK pathway.
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