沉香
细胞凋亡
牛磺胆酸
脱氧胆酸
切碎
未折叠蛋白反应
程序性细胞死亡
活力测定
药理学
化学
胆汁酸
生物
生物化学
医学
病理
替代医学
作者
Jiale Ma,Hui-Xia Huo,Hang Zhang,Lingxiao Wang,Yingxin Meng,Feng-Yu Jin,Xinyu Wang,Yimu Zhao,Pengfei Tu,Yu Song,Jiao Zheng,Jun Li
出处
期刊:Phytomedicine
[Elsevier]
日期:2022-04-01
卷期号:98: 153935-153935
被引量:6
标识
DOI:10.1016/j.phymed.2022.153935
摘要
Injury of gastric epithelial cells is one of the most important pathological features of bile reflux gastritis. Chinese agarwood (the resinous heartwood of Aquilaria sinensis) has been used to treat stomach problems for thousands of years in China. However, the pathological mechanism of epithelial cells death induced by bile acids and the therapeutic target of Chinese agarwood for improving bile reflux gastritis have not yet been fully clarified.This study aimed to investigate the pro-apoptotic effect of taurocholic acid (TCA) by regulating the ER stress pathway. Moreover, the role of Chinese agarwood 2-(2-phenylethyl)chromone-enriched extract (CPE) to inhibit gastric epithelial cell death induced by TCA was also been demonstrated.We adopted human gastric epithelial GES-1 cells to explore the mechanism of TCA-induced cell death in vitro. Then the cell viability, apoptosis rate, and protein expressions were evaluated to explore the protective effects of CPE on GES-1 cells by TCA injury. The therapeutic effect of CPE on bile reflux gastritis was further confirmed by the bile reflux mice in vivo.Our results demonstrated that TCA activated GES-1 cell apoptosis by increased cleavage of caspase-7 and PARP. Further experiments showed that TCA up-regulated endoplasmic reticulum (ER) stress, subsequently triggered the apoptosis of the epithelial cells. Our research explored that CPE is the main effective fraction in Chinese agarwood by preventing the TCA-induced gastric epithelial cell injury. CPE effectively suppressed GES-1 cell apoptosis activated by TCA through inhibiting Perk/eIF2α/CHOP pathway. The anti-apoptotic effect of CPE on gastric mucosa had also been confirmed in vivo. Moreover, the main effective components in CPE corresponding to the protection of epithelial cells were also been identified.Our finding suggested that CPE recovered the TCA-induced epithelial cell apoptosis by mediating the activation of ER stress, which explored potential medicine to treat bile reflux gastritis.
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