Abstract
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.
Highlights
Intestinal epithelial cells are the key components of the epithelial lining
Changes in intestinal epithelial barrier permeability incite mucosal inflammation leading to intestinal diseases, such as inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), irritable bowel syndrome (IBS), and colon cancer (CRC) [2,3,4]
The cell viability in Caco-2 cells was significantly inhibited by Sinapic acid (SA) treatment for 48 h, which effect was in a concentration-dependent manner (p < 0:05)
Summary
The intact intestinal epithelial maintains the intestinal physical barrier and plays a critical role in the body’s defense functions [1]. Changes in intestinal epithelial barrier permeability incite mucosal inflammation leading to intestinal diseases, such as inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), irritable bowel syndrome (IBS), and colon cancer (CRC) [2,3,4]. Intestinal epithelial barriers are formed by tight junction (TJ) proteins, including occludin, claudin, and zonula occludens (ZO), that connect the cytoskeleton and signalling molecules [5]. Intestinal inflammation has been proved to be associated with the intestinal epithelial barrier disruption [6].
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