Wheat-Grain Moxibustion Ameliorates Ulcerative Colitis: Suppressing Intestinal Inflammation, Modulating Gut Microbiota, and Restoring Mucosal Barrier Integrity.

IF 4.1 2区 医学 Q2 IMMUNOLOGY
Journal of Inflammation Research Pub Date : 2025-09-12 eCollection Date: 2025-01-01 DOI:10.2147/JIR.S540574
Tao Zhu, Shi-Yue Sun, Shuo-Xin Yang, Yu-Fang Ji, Hong-Ye Wan, Lai-Xi Ji
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引用次数: 0

Abstract

Background: Wheat-grain moxibustion (Wgm), a specialized form of moxibustion therapy, exerts therapeutic effects by delivering thermal stimulation from ignited moxa wool to specific acupoints, thereby preventing or treating various diseases. Previous studies have demonstrated its beneficial role in ulcerative colitis (UC); however, the exact mechanisms involved remain to be elucidated. This study investigated the therapeutic effects of Wgm at Zhongwan (CV12), Tianshu (ST25), and Shangjuxu (ST37) sites on colonic inflammatory cytokines, intestinal mucosal barrier homeostasis, and gut microbiome profiles in UC mice.

Materials and methods: A DSS-induced UC mouse model was established and Wgm at Zhongwan (CV12), Tianshu (ST25), and Shangjuxu (ST37) acupoints was conducted once a day for 7 consecutive days. The therapeutic effects of Wgm were assessed by monitoring body weight variations, disease activity index (DAI) scoring, colon length measurements, and histopathological features of colonic tissues, and the expression levels of inflammatory cytokines and intestinal mucosal barrier-related factors in colonic tissues were measured using enzyme-linked immunosorbent assay (ELISA), immunohistochemistry (IHC), Western blotting (WB), and real-time quantitative polymerase chain reaction (RT-PCR). Additionally, 16S rRNA sequencing was performed to characterize the gut microbial community structure and diversity.

Results: Wgm applied to Zhongwan (CV12), Tianshu (ST25), and Shangjuxu (ST37) significantly reduced the DAI and histological scores of colonic tissue in UC mice, while demonstrating specific efficacy in increasing body weight and colon length. By inhibiting the TLR4/MyD88/NF-κB signaling pathway, Wgm suppressed the release of intestinal inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α, MPO, and COX2), downregulated intestinal injury markers (DAO, D-LA, ICAM-1, and IFABP), and upregulated mucosal barrier proteins (MUC2, ZO-1, Occludin, Claudin 1), thereby restoring intestinal mucosal barrier function and restoring the composition and diversity of the gut microbiota.

Conclusion: Our results suggest that Wgm alleviates colitis by suppressing the TLR4/MyD88/NF-κB signaling pathway, reducing pro-inflammatory cytokine release, restoring intestinal mucosal barrier integrity, and modulating gut microbiome profiles. These findings collectively elucidate the potential therapeutic mechanisms by which Wgm ameliorates UC pathogenesis and demonstrate its multimodal regulatory effects in UC.

小麦艾灸改善溃疡性结肠炎:抑制肠道炎症,调节肠道微生物群,恢复粘膜屏障完整性。
背景:麦粒艾灸是一种特殊的艾灸疗法,它通过点燃的艾毛向特定的穴位传递热刺激来发挥治疗作用,从而预防或治疗各种疾病。先前的研究已经证明其在溃疡性结肠炎(UC)中的有益作用;然而,所涉及的确切机制仍有待阐明。本研究探讨了Wgm在中脘(CV12)、天枢(ST25)和上巨虚(ST37)部位对UC小鼠结肠炎性细胞因子、肠黏膜屏障稳态和肠道微生物群的治疗作用。材料与方法:建立dss诱导UC小鼠模型,在中脘穴(CV12)、天枢穴(ST25)、上巨虚穴(ST37)进行Wgm,每天1次,连续7 d。通过监测体重变化、疾病活动性指数(DAI)评分、结肠长度测量和结肠组织病理学特征来评估Wgm的治疗效果,并使用酶联免疫吸附试验(ELISA)、免疫组织化学(IHC)、Western blotting (WB)和实时定量聚合酶链反应(RT-PCR)检测结肠组织中炎症因子和肠黏膜屏障相关因子的表达水平。此外,我们还进行了16S rRNA测序来表征肠道微生物群落结构和多样性。结果:Wgm应用于中丸(CV12)、天舒(ST25)和上巨虚(ST37)可显著降低UC小鼠的DAI和结肠组织组织学评分,同时对体重和结肠长度有特定的增加作用。Wgm通过抑制TLR4/MyD88/NF-κB信号通路,抑制肠道炎症因子(IL-1β、IL-6、IL-8、TNF-α、MPO、COX2)的释放,下调肠道损伤标志物(DAO、D-LA、ICAM-1、IFABP),上调粘膜屏障蛋白(MUC2、ZO-1、Occludin、Claudin 1),从而恢复肠道黏膜屏障功能,恢复肠道微生物群的组成和多样性。结论:我们的研究结果表明,Wgm通过抑制TLR4/MyD88/NF-κB信号通路,减少促炎细胞因子释放,恢复肠黏膜屏障完整性,调节肠道微生物群谱,减轻结肠炎。这些发现共同阐明了Wgm改善UC发病机制的潜在治疗机制,并证明了其在UC中的多模式调节作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Inflammation Research
Journal of Inflammation Research Immunology and Microbiology-Immunology
CiteScore
6.10
自引率
2.20%
发文量
658
审稿时长
16 weeks
期刊介绍: An international, peer-reviewed, open access, online journal that welcomes laboratory and clinical findings on the molecular basis, cell biology and pharmacology of inflammation.
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