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短链脂肪酸在炎症性肠病中的调控作用。

Regulatory role of short-chain fatty acids in inflammatory bowel disease.

机构信息

Clinical Medical College, Yangzhou University, Yangzhou, Jiangsu Province, People's Republic of China.

Department of General Surgery, Institute of General Surgery, Clinical Medical College, Yangzhou University, Northern Jiangsu People's Hospital, Yangzhou, 225001, People's Republic of China.

出版信息

Cell Commun Signal. 2022 May 11;20(1):64. doi: 10.1186/s12964-022-00869-5.

Abstract

Inflammatory bowel disease (IBD) comprises a group of chronic inflammatory disorders of the gastrointestinal tract. Accumulating evidence shows that the development of IBD is always accompanied by the dysbiosis of the gut microbiota (GM), causing a decrease in prebiotic levels and an increase in harmful metabolite levels. This leads to persistent immune response and inflammation in the intestine, greatly impairing the physiological function of the gastrointestinal tract. Short-chain fatty acids (SCFAs) are produced by probiotic gut bacteria from a fiber-rich diet that cannot be digested directly. SCFAs with significant anti-inflammatory functions regulate immune function and prevent an excessive immune response, thereby delaying the clinical progression of IBD. In this review, we summarize the generation of SCFAs and their potential therapeutic effects on IBD. Furthermore, we suggest that SCFAs may modulate innate immune recognition and cytokine production to intervene in the progression of IBD. Additional randomized controlled trials and prospective cohort studies should also investigate the clinical impact of SCFA. Video Abstract.

摘要

炎症性肠病(IBD)是一组胃肠道慢性炎症性疾病。越来越多的证据表明,IBD 的发展总是伴随着肠道微生物群(GM)的失调,导致益生元水平降低和有害代谢物水平升高。这导致肠道持续的免疫反应和炎症,极大地损害了胃肠道的生理功能。短链脂肪酸(SCFAs)是由富含纤维的饮食不能直接消化的益生菌肠道细菌产生的。具有显著抗炎功能的 SCFAs 调节免疫功能并防止过度的免疫反应,从而延缓 IBD 的临床进展。在这篇综述中,我们总结了 SCFAs 的产生及其对 IBD 的潜在治疗作用。此外,我们认为 SCFAs 可能通过调节先天免疫识别和细胞因子产生来干预 IBD 的进展。还应进行更多的随机对照试验和前瞻性队列研究,以探讨 SCFA 的临床影响。视频摘要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e426/9097439/9a9f88463f0a/12964_2022_869_Fig1_HTML.jpg

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