Han Han, Xu Lili, Xiong Kai, Zhang Tong, Wang Zhengtao
Experiment Center for Teaching and Learning, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Cell Physiol Biochem. 2018;49(4):1304-1319. doi: 10.1159/000493409. Epub 2018 Sep 17.
BACKGROUND/AIMS: Cholestasis is the major cause of the accumulation of bile acids and results in liver damage, fibrosis, and failure. A growing number of studies have shown that gentiopicroside is a promising prospect that may protect the liver. However, its therapeutic mechanism has not yet been clarified. This study aimed to explore the effect and mechanism of gentiopicroside in cholestasis induced by alpha-naphthylisothiocyanate.
We performed isobaric tags for relative and absolute quantification-based quantitative proteomics and metabolomics using liquid chromatography quadruple time-of-fight mass spectrometry and identified the expression of 73 metabolites and 84 proteins associated with cholestasis-related dysfunctions in the metabolism of bile acids, fatty acids, and glycerophospholipids.
Integrated analyses of proteomic and metabonomic studies showed altered pathways in cholestasis-induced liver injury involving increased activity of farnesoid X receptor/retinoid X receptor, bile acid biosynthesis, and peroxisome proliferator-activated receptor-α/retinoid X receptor-α. Gentiopicroside could reverse these metabolite, protein, and blood biochemical indices, as well as alleviate liver damage. The progressive changes in the proteins and genes may be correlated with cholestasis and were confirmed by western blot and quantitative realtime polymerase chain reaction.
Gentiopicroside could be used to protect the liver in the presence of cholestasis.
背景/目的:胆汁淤积是胆汁酸蓄积的主要原因,可导致肝损伤、纤维化和肝功能衰竭。越来越多的研究表明,龙胆苦苷有望成为肝脏保护剂。然而,其治疗机制尚未阐明。本研究旨在探讨龙胆苦苷对α-萘异硫氰酸酯诱导的胆汁淤积的作用及机制。
我们采用液相色谱-四极杆飞行时间质谱联用技术,基于相对和绝对定量的等压标签进行定量蛋白质组学和代谢组学研究,鉴定了73种代谢物和84种与胆汁酸、脂肪酸和甘油磷脂代谢中胆汁淤积相关功能障碍有关的蛋白质的表达。
蛋白质组学和代谢组学研究的综合分析表明,胆汁淤积诱导的肝损伤中存在途径改变,包括法尼醇X受体/视黄醇X受体活性增加、胆汁酸生物合成以及过氧化物酶体增殖物激活受体-α/视黄醇X受体-α。龙胆苦苷可逆转这些代谢物、蛋白质和血液生化指标,并减轻肝损伤。蛋白质和基因的渐进性变化可能与胆汁淤积相关,并通过蛋白质印迹和定量实时聚合酶链反应得到证实。
龙胆苦苷可用于在胆汁淤积情况下保护肝脏。