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OBJECTIVE: To investigate the inhibitory effect of Panax notoginseng saponins(PNS) on liver fibrosis and explore the underlying mechanisms.METHODS: 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 Ι m RNA expression were determined by reverse transcriptase-polymerase chain reaction(RT-PCR). Meanwhile, the protein expression levels of α-SMA, collagen Ι, 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: 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: PNS can relieve liver fibrosis by modulating Jak2/Stat3 signaling transduction pathway, which may be one of its mechanisms to suppress hepatic fibrosis.
OBJECTIVE: To investigate the inhibitory effect of Panax notoginseng saponins (PNS) on liver fibrosis and explore the underlying mechanisms. METHODS: 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 Ι m RNA expression were determined by reverse transcriptase- ). Meanwhile, the protein expression levels of α-SMA, collagen Ι, phosphorylation-Janus activated kinase signal transducer (p-Jak2) / Jak2, and phosphorylation- activator of transcription / or immunoblotting.RESULTS: PNS treatment significantly improved the liver function of rats as indicated by decreased serum enzymatic activities of alanine aminotransferase and aspartate aminotransferase. Histopathological results indicat ed that PNS significantly reduced liver hydroxyproline and significantly attenuated expressions of collagen I, a-SMA, TGF-β1, p-Jak2 / Jak2, and p-Stat3 / Stat3 in the rat liver fibrosis model and HSCs.CONCLUSION: PNS can relieve liver fibrosis by modulating Jak2 / Stat3 signaling transduction pathway, which may be one of its mechanisms to suppress hepatic fibrosis.