Objective:To investigate the role of advanced oxidation protein products (AOPPs) in epithelial - mesenchymal transition (EMT) of small intestinal epithelial cells, and provide basis for the study of mechanism of intestinal fibrosis (IF) in intestinal bowel disease (IBD) .Methods:The small intestinal crypt epithelial cells IEC-6 were cultured in vitro. AOPPs was made by hypochlorous acid oxidation of rat serum albumin (RSA) in vitro. IEC-6 cells were divided into blank control group, AOPPs group and RSA group. The different concentrations (50, 100, 200, 400 μg/ml) of AOPPs were used to interfere with IEC-6 cells respectively in AOPPs group, 50, 100, 200, 400 μg/ml RSA were used to interfere with IEC-6 cells respectively in RSA group and no intervention in blank control group. The morphological changes of IEC-6 cells were observed and apoptosis was detected by flow cytometry in 3 groups 24 h after intervention. When the apoptosis rate was highest, the concentration of AOPPs were analyzed statistically and used to interfere IEC-6 for 48 and 72 h. The difference of apoptosis rate were analyzed between the different times. The mRNA expression of E-cadherin, Fibronectin, Snail, Slug and Collagen Ⅰ were detected in blank control group, AOPPs group and RSA group by fluorescence quantitative PCR.Results:AOPPs could induce the apoptosis of IEC-6 cells with time- and concentration-dependent effects ( P<0.05) . The apoptosis rate was (17.30 ± 1.03) %, which reached the peak by the intervention of 400 μg/ml AOPPs for 72 h. AOPPs significantly decreased the mRNA expression of E-cadherin in IEC-6 cells, significantly increased the mRNA expression of Fibronectin and CollagenⅠ, and significantly increased the mRNA expression of transcription factor Snail and Slug (all P<0.05) . Conclusions:AOPPs can promote the ECT of small intestinal epithelial cells and play a role in IF of IBD by inducing the apoptosis of IEC-6 cells, inhibiting of the transcription of E-cadherin, up-regulating the gene expression of the transcription factors Snail and Slug, while increasing the gene expression of Fibronectin and CollagenⅠ.

Objective:To investigate the role of advanced oxidation protein products (AOPPs) in epithelial - mesenchymal transition (EMT) of small intestinal epithelial cells, and provide basis for the study of mechanism of intestinal fibrosis (IF) in intestinal bowel disease (IBD) .Methods:The small intestinal crypt epithelial cells IEC-6 were cultured in vitro. AOPPs was made by hypochlorous acid oxidation of rat serum albumin (RSA) in vitro. IEC-6 cells were divided into blank control group, AOPPs group and RSA group. The different concentrations (50, 100, 200, 400 μg/ml) of AOPPs were used to interfere with IEC-6 cells respectively in AOPPs group, 50, 100, 200, 400 μg/ml RSA were used to interfere with IEC-6 cells respectively in RSA group and no intervention in blank control group. The morphological changes of IEC-6 cells were observed and apoptosis was detected by flow cytometry in 3 groups 24 h after intervention. When the apoptosis rate was highest, the concentration of AOPPs were analyzed statistically and used to interfere IEC-6 for 48 and 72 h. The difference of apoptosis rate were analyzed between the different times. The mRNA expression of E-cadherin, Fibronectin, Snail, Slug and Collagen Ⅰ were detected in blank control group, AOPPs group and RSA group by fluorescence quantitative PCR.Results:AOPPs could induce the apoptosis of IEC-6 cells with time- and concentration-dependent effects ( P<0.05) . The apoptosis rate was (17.30 ± 1.03) %, which reached the peak by the intervention of 400 μg/ml AOPPs for 72 h. AOPPs significantly decreased the mRNA expression of E-cadherin in IEC-6 cells, significantly increased the mRNA expression of Fibronectin and CollagenⅠ, and significantly increased the mRNA expression of transcription factor Snail and Slug (all P<0.05) . Conclusions:AOPPs can promote the ECT of small intestinal epithelial cells and play a role in IF of IBD by inducing the apoptosis of IEC-6 cells, inhibiting of the transcription of E-cadherin, up-regulating the gene expression of the transcription factors Snail and Slug, while increasing the gene expression of Fibronectin and CollagenⅠ.