Apigenin alleviates dextran sulfate sodium-induced ulcerative colitis via regulation of endoplasmic reticulum stress in goblet cells

IF 4.7 2区医学 Q2 IMMUNOLOGY

International immunopharmacology Pub Date : 2025-07-03 DOI:10.1016/j.intimp.2025.115164

Zhong-Hao Ji , Hai-Xiang Guo , Bingbing Wang , Wen-Zhi Ren , Jin-Ping Hu , Chengzhen Chen , Bao Yuan

引用次数: 0

Abstract

Ulcerative colitis (UC) significantly impairs quality of life and incurs substantial economic costs. Apigenin, a flavonoid abundant in fruits and vegetables, has demonstrated potential in UC management. Utilizing DSS-induced UC mouse models and LS 174 T goblet cell models, this study elucidates apigenin's protective mechanisms. Dietary supplementation with 40 mg/kg apigenin markedly alleviated UC symptoms. Antibiotic-mediated microbiota depletion confirmed that apigenin's efficacy is independent of gut microbiota. Mechanistically, apigenin enhances SERCA2 expression to maintain intracellular calcium homeostasis, thereby inhibiting excessive activation of the PERK-eIF2α-ATF4-CHOP pathway, reducing goblet cell apoptosis, and preserving mucosal barrier integrity. These findings provide a robust theoretical foundation for apigenin as a dietary supplement in the prevention and mitigation of colitis.

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芹菜素通过调节杯状细胞内质网应激减轻葡聚糖硫酸钠诱导的溃疡性结肠炎

溃疡性结肠炎（UC）严重影响生活质量，并造成巨大的经济损失。芹菜素是一种富含水果和蔬菜的类黄酮，在UC管理中具有潜力。本研究利用dss诱导UC小鼠模型和ls174 T杯状细胞模型，阐明芹菜素的保护机制。饲粮中添加40 mg/kg芹菜素可显著缓解UC症状。抗生素介导的微生物群消耗证实了芹菜素的功效与肠道微生物群无关。机制上，芹菜素通过增强SERCA2表达维持细胞内钙稳态，从而抑制PERK-eIF2α-ATF4-CHOP通路的过度激活，减少杯状细胞凋亡，保持粘膜屏障的完整性。这些发现为芹菜素作为预防和缓解结肠炎的膳食补充剂提供了坚实的理论基础。

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来源期刊

International immunopharmacology 医学-免疫学

CiteScore

8.40

自引率

3.60%

发文量

935

审稿时长

53 days

期刊介绍： International Immunopharmacology is the primary vehicle for the publication of original research papers pertinent to the overlapping areas of immunology, pharmacology, cytokine biology, immunotherapy, immunopathology and immunotoxicology. Review articles that encompass these subjects are also welcome. The subject material appropriate for submission includes: • Clinical studies employing immunotherapy of any type including the use of: bacterial and chemical agents; thymic hormones, interferon, lymphokines, etc., in transplantation and diseases such as cancer, immunodeficiency, chronic infection and allergic, inflammatory or autoimmune disorders. • Studies on the mechanisms of action of these agents for specific parameters of immune competence as well as the overall clinical state. • Pre-clinical animal studies and in vitro studies on mechanisms of action with immunopotentiators, immunomodulators, immunoadjuvants and other pharmacological agents active on cells participating in immune or allergic responses. • Pharmacological compounds, microbial products and toxicological agents that affect the lymphoid system, and their mechanisms of action. • Agents that activate genes or modify transcription and translation within the immune response. • Substances activated, generated, or released through immunologic or related pathways that are pharmacologically active. • Production, function and regulation of cytokines and their receptors. • Classical pharmacological studies on the effects of chemokines and bioactive factors released during immunological reactions.