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The modulatory effect of triclosan on the reversion of the activated phenotype of LX-2 hepatic stellate cells

机译:三氯烷对LX-2肝星状细胞活性表型逆转的调节作用

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Hepatic diseases leading to fibrosis affect millions of individuals worldwide and are a major public health challenge. Although, there have been many advances in understanding hepatic fibrogenesis, an effective therapy remains elusive. Studies focus primarily on activation of the hepatic stellate cells (HSCs), the principal fibrogenic cells in the liver; however, fewer numbers of studies have examined molecular mechanisms that deactivate HSC, controlling the profibrogenic phenotype. In the present study, we evaluated cellular and molecular actions of the chemical triclosan (TCS) in reverting activated HSCs to a quiesced phenotype. We demonstrated that the inhibition of the enzyme fatty acid synthase by TCS in activated HSCs promotes survival of the cells and triggers cellular and molecular changes that promote cellular phenotypic reversion, offering potentially new therapeutic directions.
机译:导致肝纤维化的肝病影响着全世界数百万人,是一个重大的公共卫生挑战。尽管在了解肝纤维化方面取得了许多进展,但有效的治疗方法仍然难以捉摸。研究主要集中于肝星状细胞(HSC)的激活,HSC是肝脏中主要的纤维化细胞;然而,研究使HSC失活的分子机制、控制促纤维化表型的研究较少。在本研究中,我们评估了化学三氯生(TCS)在将活化的HSC恢复为静止表型方面的细胞和分子作用。我们证明,TCS对激活的HSC中的脂肪酸合成酶的抑制促进了细胞的存活,并触发了促进细胞表型逆转的细胞和分子变化,从而提供了潜在的新治疗方向。

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