期刊
MEDIATORS OF INFLAMMATION
卷 2014, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2014/901530
关键词
-
资金
- National Natural Science Foundation of China [NSFC 81071532, NSFC 81370479, NSFC 81330013]
- Program for Changjiang Scholars and Innovative Research Team in University [IRT 13050]
Intestinal ischemic reperfusion (I/R) can cause dysfunction of the intestinal mucosal barrier; however, the mechanism of the intestinal mucosal barrier dysfunction caused by I/R remains unclear. In this study, using intestinal epithelial cells under anaerobic cultivation and an in vivo rat intestinal I/R model, we found that hypoxia and I/R increased the expression of BMP2/4 and upregulated BMP type Ia receptor and BMP type II receptor expression. We also found that exogenous BMP2/4 can activate the ERK and AKT signaling pathways in rat small intestine (IEC-6) cells, thereby activating NF-kappa B signaling, which leads to increased levels of inflammatory factors, such as TNF-alpha and IL-6. Furthermore, recombinant BMP2/4 decreased the expression of the tight junction protein occludin via the activation of the NF-kappa B pathway; these effects were abolished by treatment with the BMP-specific antagonist noggin or the NF-kappa B inhibitor pyrrolidine dithiocarbamate (PDTC). All these factors can destroy the intestinal mucosal barrier, thereby leading to weaker barrier function. On the basis of these data, we conclude that BMP2/4 may act as the pathogenic basis for intestinal mucosal barrier dysfunction when the intestines suffer an I/R injury. Our results provide background for the development pharmacologic interventions in the management of I/R injury.
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