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Wedelolactone is a major coumarin of Ecliptaprostrata, which is used for preventing liver damage.However the effects ofwedelolactone on hepatic fibrosis remained unexplored.The purpose of this study was to demonstrate the anti-fibrotic effects of wedelolactone on activated human hepatic stellate cell (HSC) line LX-2 and the possible underlying mechanisms by means of MTT assay, Hoechst staining, as well as real-time quantitative PCR and western blot.The results showed that wedelolactone reduced the cellular viability of LX-2 in a time and dose-dependent manner.After treatment of wedelolactone, the expressions of collagen 1 and α-smooth muscle actin, two biomarkers of LX-2 activation, were remarkably decreased.The apoptosis of LX-2 cells was induced by wedelolactone accompanied with the decreasing expression of anti-apoptotic Bcl-2 and increasing expression of pro-apoptotic Bax.In addition, phosphorylated status of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) was up-regulated, but not in p38.Moreover, wedelolactone significantly repressed the level of phosphorylated inhibitor of nuclear factorκB(lκ B) and p65 in nucleus in spite of tumor necrosis factor-αstimulation.In conclusion, wedelolactone could significantly inhibit the activation of LX-2 cells, the underlying mechanisms of which included inducing Bcl-2 family involved apoptosis, up-regulating phosphorylated status of ERK and JNK expressions, and inhibiting nuclear factor-κB (NF-κB) mediated activity.Wedelolactone might present as a useful tool for the prevention and treatment of hepatic fibrosis.