Hepatoprotective effects of berberine on liver fibrosis via activation of AMP-activated protein kinase

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• 作者：Jing Li^a ; Yue Pan^a ; Mujie Kan^a ; Xuanang Xiao^a ; Yunjing Wang^a ; Fengying Guan^a ; Xuewen Zhang^b ; ^{zxw515@sohu.com" class="auth_mail} ; Li Chen^a ; ^{zhouweichen@yahoo.com" class="auth_mail}
• 关键词：BBR ; berberine ; AMPK ; AMP-activated protein kinase ; HSC ; hepatic stellate cells ; TGF ; transforming growth factor ; ROS ; reactive oxygen species ; CCl4 ; carbon tetrachloride (CCl4)
• 刊名：Life Sciences
• 出版年：7 March, 2014
• 年：2014
• 卷：98
• 期：1
• 页码：24-30
• 全文大小：850 K

文摘

Aims

We investigated the protective effect of berberine (BBR) on chronic liver fibrosis in mice and the potential mechanism underlying the activation of AMP-activated protein kinase (AMPK) pathway.

Main methods

CCl4-induced chronic liver fibrosis model in mice was established and activated rat hepatic stellate cell was treated with BBR. Cell viability was evaluated by SRB assay and protein expressions were detected by Western blot.

Key findings

Our results showed that BBR ameliorated the liver fibrosis in mice with CCl4-induced liver injury and inhibited the proliferation of hepatic stellate cell in dose- and time-dependent manner. BBR decreased the enzyme release of ALT, AST, and ALP in serum, elevated SOD and reduced MDA content of liver tissue in CCl4-induced liver fibrosis model. BBR delayed the formation of regenerative nodules and reduced necrotic areas compared to CCl4 group. Moreover, BBR treatment activated AMPK, decreased the protein expression of Nox4, TGF-尾1 and the phosphorylated Akt. The expression of smooth muscle actin (伪-SMA), the marker of activated hepatic stellate cell, was also reduced by BBR treatment.

Significance

Our studies firstly demonstrated that BBR exerted hepatoprotective effects possibly via activation of AMPK, blocking Nox4 and Akt expression. Our findings may benefit the development of new strategies in the prevention of chronic liver disease.