Panax notoginseng saponins ameliorates experimental hepatic fibrosis and hepatic stellate cell proliferation by inhibiting the Jak2/Stat3 pathways

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• 作者：Jiang Hui^a ; ^b ; Gao Jiarong^a ; ^b ; ^{China.jhanbing@163.com" class="auth_mail" title="E-mail the corresponding author} ; Wang Yongzhong^a ; ^b ; Zhang Jiafu^a ; ^b ; Han Yanquan^a ; ^b ; Wei Liangbing^a ; ^b ; Liu Xiaochuang^a ; ^b ; Wu Jian^a ; ^b
• 关键词：Sanchinoside ; Liver fibrosis ; Carbon tetrachloride ; Hepatic stellate cells ; Jak2/Stat3 pathway
• 刊名：Journal of Traditional Chinese Medicine
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：36
• 期：2
• 页码：217-224
• 全文大小：5948 K

文摘

To investigate the inhibitory effect of Panax notoginseng saponins (PNS) on liver fibrosis and explore the underlying mechanisms.

Methods

170">Carbon tetrachloride (CCl₄)-treated rats and hepatic stellate cells (HSCs) were used. The effect of PNS on CCl₄-induced liver fibrosis was studied with histochemical and biochemical analysis. Transforming growth factor (TGF)-β1, α-smooth muscle actin (α-SMA), and collagen I mRNA expression were determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Meanwhile, the protein expression levels of α-SMA, collagen I, phosphorylation-Janus activated kinase signal transducer (p-Jak2) / Jak2, and phosphorylation-activator of transcription (p-Stat)3 / Stat3 were determined by immunohistochemistry and / or immunoblotting.

Results

180">PNS treatment significantly improved the liver function of rats as indicated by decreased serum enzymatic activities of alanine aminotransferase and aspartate aminotransferase. Histopathological results indicated that PNS alleviated liver damage and reduced the formation of fibrous septa. Moreover, PNS significantly decreased liver hydroxyproline and significantly attenuated expressions of collagen I, α-SMA, TGF-β1, p-Jak2 / Jak2, and p-Stat3 / Stat3 in the rat liver fibrosis model and HSCs.

Conclusion

190">PNS can relieve liver fibrosis by modulating Jak2/Stat3 signaling transduction pathway, which may be one of its mechanisms to suppress hepatic fibrosis.