封堵器
炎症
紧密连接
势垒函数
肠道通透性
体内
胱硫醚β合酶
化学
炎症性肠病
碳酸钙-2
体外
胱硫醚γ裂解酶
免疫学
细胞生物学
医学
生物
生物化学
病理
酶
疾病
生物技术
半胱氨酸
作者
Hongyu Zhao,Rui Yan,Xiaogang Zhou,Fang Ji,Bing Zhang
标识
DOI:10.1016/j.intimp.2016.07.020
摘要
Intestinal barrier involves in the pathogeny of inflammatory bowel disease (IBD) and hydrogen sulfide (H2S) has been reported to improve intestinal barrier integrity. Thus, this study investigated the effects of GYY4137, a slow-release H2S donor, on DSS-induced inflammation and intestinal dysfunction. In vitro model, cellular permeability was significantly increased and expression of tight junctions (ZO-1, Cauldin4, and Occludin) was downregulated in Caco-2 cells. GYY4137 treatment markedly attenuated DSS-induced inflammation and barrier dysfunction. Cystathionine β-synthase (CBS)-siRNA transfection further demonstrated that endogenous H2S system involves in DSS-induced inflammation and mediates barrier function. In vivo model, DSS exposure caused colonic inflammation and injury in mice and GYY4137 injection alleviated inflammatory response and improved intestinal barrier via reducing intestinal permeability and upregulating of tight junctions. In conclusion, endogenous H2S system involves in DSS-induced inflammation and H2S addition alleviated inflammation and intestinal dysfunction in vitro and in vivo.
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