黄金双肾汤通过抑制TNF/NF-κB信号传导和促进CFTR相关的胃黏膜屏障修复来缓解慢性萎缩性胃炎
Huangjin Shuangshen decoction alleviates chronic atrophic gastritis by suppressing TNF/NF-κB signaling and promoting CFTR-associated gastric mucosal barrier repair.
摘要(中文译文)
慢性萎缩性胃炎（CAG）是一种癌前胃部病变，以持续性炎症损伤、腺体萎缩及胃黏膜屏障相关完整性受损为特征。黄金双参汤（HJSS）在胃炎相关疾病中显示出治疗潜力，但其对CAG的作用及潜在机制尚不明确。本研究探讨HJSS是否通过调节炎症相关屏障功能障碍来缓解CAG。采用MNNG联合雷尼替丁及不规则喂养诱导小鼠CAG模型，随后给予不同剂量HJSS治疗，并以叶酸作为阳性对照。评估了组织病理学、胃功能指标、炎症介质、凋亡相关标志物及屏障相关分子。采用HJSS含药血清处理MNNG损伤的GES-1细胞进行验证。整合转录组学分析、网络药理学及药理学抑制实验探讨潜在机制。HJSS可减轻实验性CAG的胃黏膜萎缩及组织病理学损伤，改善胃功能损害，降低炎症负荷，并减轻凋亡相关上皮损伤。HJSS还促进胃黏膜屏障相关分子的恢复，包括CFTR、ZO-1、MUC5AC、Occludin和Claudin-1。转录组学与网络药理学的整合分析突显了涉及TNF相关信号及CFTR相关调控的炎症-屏障框架。HJSS减轻MNNG诱导的上皮损伤，而CFTR抑制则削弱了HJSS相关的CFTR和ZO-1恢复。HJSS还与TNF/NF-κB信号抑制及p65核转位减少相关。HJSS通过减轻炎症损伤并促进胃黏膜屏障相关分子特征的恢复来缓解MNNG诱导的CAG。其保护作用与抑制TNF/NF-κB信号及CFTR相关调控的参与有关，支持HJSS作用于CAG的炎症-屏障机制。
Abstract
Chronic atrophic gastritis (CAG) is a precancerous gastric lesion characterized by persistent inflammatory injury, glandular atrophy, and impairment of gastric mucosal barrier-associated integrity. Huangjin Shuangshen Decoction (HJSS) has shown therapeutic potential in gastritis-related disorders, but its effects on CAG and the underlying mechanism remain unclear. This study investigated whether HJSS alleviates CAG by modulating inflammation-associated barrier dysfunction. CAG was induced in mice by MNNG combined with ranitidine and irregular feeding, followed by treatment with different doses of HJSS, with folic acid as a positive control. Histopathology, gastric function indices, inflammatory mediators, apoptosis-related markers, and barrier-associated molecules were assessed . MNNG-injured GES-1 cells treated with HJSS-medicated serum were used for validation. Transcriptomic analysis, network pharmacology, and pharmacological inhibition were integrated to explore the underlying mechanisms. HJSS alleviated gastric mucosal atrophy and histopathological injury, improved gastric functional impairment, reduced inflammatory burden, and attenuated apoptosis-associated epithelial injury in experimental CAG. HJSS also promoted the recovery of gastric mucosal barrier-associated molecules, including CFTR, ZO-1, MUC5AC, Occludin, and Claudin-1. Integrated transcriptomic and network pharmacology analyses highlighted an inflammation-barrier framework involving TNF-related signaling and CFTR-associated regulation. , HJSS mitigated MNNG-induced epithelial injury, whereas CFTR inhibition attenuated the HJSS-associated restoration of CFTR and ZO-1. HJSS was further associated with suppression of TNF/NF-κB signaling and reduced p65 nuclear translocation. HJSS alleviates MNNG-induced CAG by attenuating inflammatory injury and promoting the recovery of gastric mucosal barrier-associated molecular features. Its protective effects are associated with suppression of TNF/NF-κB signaling and involvement of CFTR-associated regulation, supporting an inflammation-barrier mechanism underlying the action of HJSS in CAG.
如何引用
AMA
Shuo Zhang, Shuya Zhang, Mengyi Wang, Xueru Huang, Chen Huang, Tao Jiang, et al. Huangjin Shuangshen decoction alleviates chronic atrophic gastritis by suppressing TNF/NF-κB signaling and promoting CFTR-associated gastric mucosal barrier repair.. Frontiers in immunology. 2026; doi:10.3389/fimmu.2026.1848471.
APA
Shuo Zhang, Shuya Zhang, Mengyi Wang, Xueru Huang, Chen Huang, Tao Jiang, et al (2026). Huangjin Shuangshen decoction alleviates chronic atrophic gastritis by suppressing TNF/NF-κB signaling and promoting CFTR-associated gastric mucosal barrier repair.. Frontiers in immunology. https://doi.org/10.3389/fimmu.2026.1848471
GB/T 7714
Shuo Zhang, Shuya Zhang, Mengyi Wang, Xueru Huang, Chen Huang, Tao Jiang, et al. Huangjin Shuangshen decoction alleviates chronic atrophic gastritis by suppressing TNF/NF-κB signaling and promoting CFTR-associated gastric mucosal barrier repair.[J]. Frontiers in immunology, 2026 doi:10.3389/fimmu.2026.1848471.
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