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Sinapic Acid Alleviated Inflammation-Induced Intestinal Epithelial Barrier Dysfunction in Lipopolysaccharide- (LPS-) Treated Caco-2 Cells
Mediators of Inflammation ( IF 4.6 ) Pub Date : 2021-09-08 , DOI: 10.1155/2021/5514075
Huan Lan 1 , Lu-Ying Zhang 2 , Wen He 2 , Wan-Ying Li 2 , Zhen Zeng 2, 3 , Bo Qian 2, 4 , Chengqiang Wang 2 , Jia-Le Song 2, 5
Affiliation  

The integrity and permeability of the intestinal epithelial barrier are important indicators of intestinal health. Impaired intestinal epithelial barrier function and increased intestinal permeability are closely linked to the onset and progression of various intestinal diseases. Sinapic acid (SA) is a phenolic acid that has anti-inflammatory, antihyperglycemic, and antioxidant activities; meanwhile, it is also effective in the protection of inflammatory bowel disease (IBD), but the specific mechanisms remain unclear. Here, we evaluated the anti-inflammatory of SA and investigated its potential therapeutic activity in LPS-induced intestinal epithelial barrier and tight junction (TJ) protein dysfunction. SA improved cell viability; attenuated epithelial permeability; restored the protein and mRNA expression of claudin-1, ZO-1, and occludin; and reversed the redistribution of the ZO-1 and claudin-1 proteins in LPS-treated Caco-2 cells. Moreover, SA reduced the inflammatory response by downregulating the activation of the TLR4/NF-κB pathway and attenuated LPS-induced intestinal barrier dysfunction by decreasing the activation of the MLCK/MLC pathway. This study demonstrated that SA has strong anti-inflammatory activity and can alleviate the occurrence of high intercellular permeability in Caco-2 cells exposed to LPS.

中文翻译:

芥子酸在脂多糖 (LPS-) 处理的 Caco-2 细胞中减轻炎症诱导的肠上皮屏障功能障碍

肠上皮屏障的完整性和通透性是肠道健康的重要指标。肠上皮屏障功能受损和肠道通透性增加与各种肠道疾病的发生和发展密切相关。芥子酸 (SA) 是一种酚酸,具有抗炎、抗高血糖和抗氧化活性;同时,对炎症性肠病(IBD)也有保护作用,但具体机制尚不清楚。在这里,我们评估了 SA 的抗炎作用,并研究了其在 LPS 诱导的肠上皮屏障和紧密连接 (TJ) 蛋白功能障碍中的潜在治疗活性。SA 提高细胞活力;上皮通透性减弱;恢复了claudin-1、ZO-1和occludin的蛋白和mRNA表达;并逆转了 LPS 处理的 Caco-2 细胞中 ZO-1 和 Claudin-1 蛋白的重新分布。此外,SA 通过下调 TLR4/NF- 的激活来降低炎症反应。κ B 通路和通过减少 MLCK/MLC 通路的激活来减轻 LPS 诱导的肠屏障功能障碍。本研究表明,SA 具有很强的抗炎活性,可以缓解暴露于 LPS 的 Caco-2 细胞中高细胞间通透性的发生。
更新日期:2021-09-08
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