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Mechanistic insights into the ameliorative effects of Xianglianhuazhuo formula on chronic atrophic gastritis through ferroptosis mediated by YY1/miR-320a/TFRC signal pathway

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机构: [1]Department of Spleen and Stomach Diseases, First Affiliated Hospital of Hebei University of Chinese Medicine, Shijiazhuang, Heibei, 050011, China. [2]Hebei Key Laboratory of Integrated Chinese and Western Medicine for Gastroenterology Research, First Affiliated Hospital of Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050011, China [3]Hebei Key Laboratory of Turbidity Toxin Syndrome, First Affiliated Hospital of Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050011, China. [4]College of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang, Heibei, 050200, China.
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关键词: Xianglianhuazhuo formula Chronic atrophic gastritis Ferroptosis YY1 miR-320a TFRC

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.Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.

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出版当年[2025]版:
大类 | 2 区 医学
小类 | 1 区 全科医学与补充医学 1 区 药学 2 区 药物化学 2 区 植物科学
最新[2025]版:
大类 | 2 区 医学
小类 | 1 区 全科医学与补充医学 1 区 药学 2 区 药物化学 2 区 植物科学
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第一作者机构: [1]Department of Spleen and Stomach Diseases, First Affiliated Hospital of Hebei University of Chinese Medicine, Shijiazhuang, Heibei, 050011, China.
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通讯作者:
通讯机构: [1]Department of Spleen and Stomach Diseases, First Affiliated Hospital of Hebei University of Chinese Medicine, Shijiazhuang, Heibei, 050011, China. [2]Hebei Key Laboratory of Integrated Chinese and Western Medicine for Gastroenterology Research, First Affiliated Hospital of Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050011, China [3]Hebei Key Laboratory of Turbidity Toxin Syndrome, First Affiliated Hospital of Hebei University of Chinese Medicine, Shijiazhuang, Hebei, 050011, China.
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