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姜黄素通过. 减轻免疫诱导的上皮屏障功能障碍。

Curcumin Mitigates Immune-Induced Epithelial Barrier Dysfunction by .

机构信息

Institute of Clinical Physiology/Nutritional Medicine, Medical Department, Division of Gastroenterology, Infectiology, Rheumatology, Charité-Universitätsmedizin Berlin, 12203 Berlin, Germany.

Institute of Microbiology, Infectious Diseases and Immunology, Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, 14195 Berlin, Germany.

出版信息

Int J Mol Sci. 2019 Sep 28;20(19):4830. doi: 10.3390/ijms20194830.

Abstract

() is the most common cause of foodborne gastroenteritis worldwide. The bacteria induce diarrhea and inflammation by invading the intestinal epithelium. Curcumin is a natural polyphenol from turmeric rhizome of , a medical plant, and is commonly used in curry powder. The aim of this study was the investigation of the protective effects of curcumin against immune-induced epithelial barrier dysfunction in infection. The indirect -induced barrier defects and its protection by curcumin were analyzed in co-cultures with HT-29/B6-GR/MR epithelial cells together with differentiated THP-1 immune cells. Electrophysiological measurements revealed a reduction in transepithelial electrical resistance (TER) in infected co-cultures. An increase in fluorescein (332 Da) permeability in co-cultures as well as in the germ-free IL-10 mouse model after infection was shown. Curcumin treatment attenuated the -induced increase in fluorescein permeability in both models. Moreover, apoptosis induction, tight junction redistribution, and an increased inflammatory response-represented by TNF-α, IL-1β, and IL-6 secretion-was observed in co-cultures after infection and reversed by curcumin. In conclusion, curcumin protects against indirect -triggered immune-induced barrier defects and might be a therapeutic and protective agent in patients.

摘要

()是全球范围内最常见的食源性肠胃炎致病菌。该细菌通过侵袭肠上皮细胞引发腹泻和炎症。姜黄素是来自姜黄根茎的天然多酚类物质,是一种药用植物,常用于咖喱粉中。本研究旨在探讨姜黄素对感染诱导的上皮屏障功能障碍的保护作用。通过与 HT-29/B6-GR/MR 上皮细胞和分化的 THP-1 免疫细胞共培养,分析间接诱导的屏障缺陷及其对姜黄素的保护作用。电生理学测量显示,感染共培养物中的跨上皮电阻(TER)降低。在感染后的无特定病原体 IL-10 小鼠模型中,共培养物和无特定病原体中的荧光素(332 Da)通透性增加。姜黄素治疗可减轻两种模型中感染引起的荧光素通透性增加。此外,在感染后共培养物中观察到细胞凋亡诱导、紧密连接重分布以及 TNF-α、IL-1β 和 IL-6 分泌增加的炎症反应,而姜黄素可逆转这种情况。综上所述,姜黄素可预防间接诱导的免疫相关屏障缺陷,可能是患者的一种治疗和保护剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ade/6802366/4253a97ed857/ijms-20-04830-g001.jpg

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