Guangxi Medical University, Nanning 530021, China.
Guangxi Medical University, Nanning 530021, China.
Int Immunopharmacol. 2019 Oct;75:105759. doi: 10.1016/j.intimp.2019.105759. Epub 2019 Jul 17.
This study aimed to investigate the effect and underlying mechanism of Methyl helicterilate from Helicteres angustifolia (MHHA) on alcohol-induced hepatic fibrosis. The results showed that MHHA treatment markedly alleviated alcohol-induced liver injury and notably reduced collagen deposition in liver tissue. It significantly enhanced the activity of alcohol dehydrogenase and aldehyde dehydrogenase. Moreover, MHHA treatment markedly decreased the content of inflammatory cytokines, alleviated collagen accumulation, and inhibited the expression of TGF-β1 and Smad2/3 in liver tissue. The experiments in cells showed that MHHA significantly inhibited HSC activation by blocking TGF-β1/Smads signaling pathway. Additionally, it notably induced HSC apoptosis by modulating the mitochondria-dependent pathway. The present study demonstrates that MHHA treatment significantly ameliorates alcoholic hepatic fibrosis and the underlying mechanism may be ascribed to the inhibition of the TGF-β1/Smads pathway and regulation of the mitochondria-mediated apoptotic pathway.
本研究旨在探讨黄麻叶甲基千里光菲灵（MHHA）对酒精性肝纤维化的作用及机制。结果表明，MHHA 治疗可显著减轻酒精性肝损伤，显著减少肝组织胶原沉积。它显著增强了醇脱氢酶和醛脱氢酶的活性。此外，MHHA 治疗可显著降低炎症细胞因子的含量，减轻胶原堆积，并抑制肝组织中 TGF-β1 和 Smad2/3 的表达。细胞实验表明，MHHA 通过阻断 TGF-β1/Smads 信号通路显著抑制 HSC 的激活。此外，它通过调节线粒体依赖性途径显著诱导 HSC 凋亡。本研究表明，MHHA 治疗可显著改善酒精性肝纤维化，其作用机制可能归因于抑制 TGF-β1/Smads 途径和调节线粒体介导的凋亡途径。
