Expression and significance of miR-142-3p in post-infectious irritable bowel syndrome

Objective To explore the expression and significance of miR-142-3p in post-infectious irritable bowel syndrome （PI-IBS）， and to further clarify the molecular mechanism of miR-142-3p in regulating the incidence and development of PI-IBS. Methods After stimulation using the lipopolysaccharide （LPS）， the effect of miR-142-3p on high mobility group box 1 （HMGB1）-toll-like receptor 4（TLR4）target genes was investigated in the rat intestinal epithelial cells. TargetScan prediction software analysis showed that HMGB1 was a target gene of miR-142-3p. Subsequently， the PI-IBS model was established using trichinella infection. Primary intestinal epithelial cells were subjected to the siRNA transfection assay. Total RNA was extracted from intestinal epithelial cells. The expression levels of miR-142-3p， HMGB1 and TLR4 mRNA in cells were quantitatively determined by real-time PCR. The effect of miR-142-3p on the HMGB1-TLR4 target genes was evaluated. The mediating role of HMGB1 in the anti-inflammation of miR-142-3p was further validated. Results Inflammatory genes NLRP3， IL-1β， IL-6， IL-18 and TNF-α were all the target genes of HMGB1-TLR4. After the LPS stimulation， administration of miR-142-3p significantly inhibited the expression levels pf HMGB1-TLR4 target genes （NLRP3， IL-1β， IL-6， IL-18 and TNF-α） （all P < 0.01）. After the targeted knockdown of HMGB1 in intestinal epithelial cells using siRNA， the HMGB1 expression level in the cells was down-regulated by more than 80%， whereas no significant changes were observed in the expression levels of HMGB1-TLR4 target genes （NLRP3， IL-1β， IL-6， IL-18 and TNF-α） （all P > 0.05）. Conclusion miR-142-3p plays an anti-inflammatory role in intestinal epithelial cells， which is dependent on HMGB1.