水解物
封堵器
碳酸钙-2
化学
脂多糖
紧密连接
蛋清
炎症
细胞生物学
促炎细胞因子
生物化学
生物
细胞
免疫学
水解
作者
Xiaoyu Bao,Jianping Wu
标识
DOI:10.1016/j.jff.2021.104822
摘要
Ovomucin-protex 26L hydrolysate could neutralize LPS and inhibit the endotoxic activities of LPS. It alleviated inflammation through MAPK and NFκB pathways, restored the expression and assembly of tight junction proteins, and benefited the barrier integrity of Caco-2 cells challenged with LPS. • Ovomucin-protex26L hydrolysate inhibited LPS-induced permeation in Caco-2 cells. • The hydrolysate restored tight junction protein expression and cell surface assembly. • The hydrolysate mitigated LPS stress and modulated NF-κB and MAPK pathways. Disruption of the intestinal barrier is closely associated with intestinal inflammation and disease development. Ovomucin is a bioactive protein in chicken egg white, and its hydrolysate has been revealed to prevent the adhesion of pathogen to intestinal epithelial cells. However, the effect of ovomucin hydrolysate on intestinal barrier integrity and associated anti-inflammation mechanism has not been demonstrated. Here, we investigated its activity in lipopolysaccharide (LPS)-induced monolayer dysfunction of differentiated Caco-2 cells to unravel the underlying molecular mechanisms. Ovomucin-protex 26L hydrolysate significantly increased transepithelial electronic resistance (TEER) values, decreased the paracellular FITC-dextran flux permeability, and recovered the expression of occludin and ZO-1 in LPS-stimulated Caco-2 cells. Meanwhile, ovomucin-protex 26L hydrolysate significantly inhibited the LPS-induced activation of NF-κB and MAPK pathways. These results suggested the ability of ovomucin-protex 26L hydrolysate to suppress LPS-induced intestinal barrier function damage via the inhibition of inflammatory responses.
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