细胞凋亡
基因沉默
癌症研究
细胞生长
体内
细胞
细胞生物学
YY1年
信号转导
萎缩性胃炎
程序性细胞死亡
体外
生物
医学
胃炎
生物化学
基因
基因表达
遗传学
胃
发起人
作者
Yuxi Guo,Xuemei Jia,Peng Du,Jie Wang,Yao Du,Bolin Liu,Yucong Xue,Jianming Jiang,Yanru Cai,Qian Yang
标识
DOI:10.1016/j.jep.2023.117608
摘要
Xianglianhuazhuo formula (XLHZ) has a potential therapeutic effect on chronic atrophic gastritis (CAG). However, the specific molecular mechanism remains unclear. To evaluate the effect of XLHZ on CAG in vitro and in vivo and its potential mechanisms. A rat model of CAG was established using a composite modeling method, and the pathological changes and ultrastructure of gastric mucosa were observed. YY1/miR-320a/TFRC and ferroptosis-related molecules were detected. An MNNG-induced gastric epithelial cell model was established in vitro to evaluate the inhibitory effect of XLHZ on cell ferroptosis by observing cell proliferation, migration, invasion, apoptosis, and molecules related to ferroptosis. The specific mechanism of action of XLHZ in treating CAG was elucidated by silencing or overexpression of targets. In vivo experiments showed that XLHZ could improve the pathological status and ultrastructure of gastric mucosa and inhibit ferroptosis by regulating the YY1/miR-320a/TFRC signaling pathway. The results in vitro demonstrated that transfection of miR-320a mimics inhibited cell proliferation, migration, and invasion while promoting cell apoptosis. MiR-320a targeted TFRC and inhibited ferroptosis. Overexpression of TFRC reversed the inhibitory effect of miR-320a overexpression on cell proliferation. The effect of XLHZ was consistent with that of miR-320a. YY1 targeted miR-320a, and its overexpression promoted ferroptosis. XLHZ inhibited ferroptosis by regulating the YY1/miR-320a/TFRC signaling pathway, ultimately impeding the progression of CAG.
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