Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology · 2019
[Downregulation of miR-129-5p alleviates alcohol-induced barrier dysfunction of Caco-2 human intestinal epithelial cells].
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Ren Li, Qv Amin, Liu Yaping, Luo Miaosha
Аннотация
Objective To investigate the effect of miR-129-5p on alcohol-induced intestinal epithelial permeability. Methods Real-time quantitative PCR was used to detect the expression level of miR-129-5p in sigmoid colon biopsies and alcohol-induced differentiated Caco-2 cells from patients with alcoholic liver disease and healthy people. Then, the differentiated Caco-2 cells were divided into 4 groups: the control group, the alcohol group (treatment with 50 mmol/L alcohol for 60 minutes), alcohol combined with miR-129-5p inhibitor group (transfection with miR-129-5p inhibitor before alcohol treatment), and alcohol combined with miR-129-5p inhibitor control group (transfection with miR-129-5p inhibitor control before alcohol treatment). After the alcohol treatment, the transepithelial electrical resistance (TER) was analyzed by a resistance meter, and the protein levels relevant to tight junction (occludin and ZO-1) were determined by Western blotting. Results The expression level of miR-129-5p was elevated in the biopsies of the patients with alcoholic liver disease compared with that in the healthy controls. Alcohol treatment increased miR-129-5p expression in the differentiated Caco-2 cells. Compared with the control group, TER and the protein levels of occludin and ZO-1 decreased in the alcohol group. Compared with the alcohol group, TER and the protein levels of occludin and ZO-1 were enhanced in the alcohol combined with miR-129-5p group; however, these changes were not altered in the alcohol combined with miR-129-5p inhibitor control group. Conclusion The miR-129-5p expression is elevated in sigmoid colon biopsies and alcohol-induced differentiated Caco-2 cells from patients with alcoholic liver disease. Inhibition of miR-129-5p can suppress alcohol-induced intestinal epithelial permeability.