Protective Effect of MicroRNA-23b on Kidney Injury in Septic Rats Through Regulation of Mothers Against Decapentaplegic Homolog 3 (Smad3)

Abstract

Our study aims to investigate the mechanism whereby microRNA (miRNA)-23b alleviates kidney damage in septic rats. Herein, we set up septic rat model, control group and sham-operated model to evaluate the kidney tissue damage. The glomerular mesangial cells isolated from rats were transfected with plasmids expressing miR-23b followed by analysis of the expression of miR-23b, Smad3, TLR4, HMGB1 and expression of autophagy-related proteins (LC3, beclin-1) by western blot and RT-qPCR. The level of TNF-α, IL-6 and BUN and SCr were significantly elevated in the model group and decreased after overexpression of miR-23b with elevated LC3-II, Smad3 and Beclin-1 expression. miR-23b mimic group presented highest expression of miR-23b, followed by miR-23b NC group, and miR-23b inhibitor group. The levels of TLR4, and HMGB1 and positive rate of NF-κBp65 in miR-23b mimic group were significantly lower than those in miR-23b inhibitor group (p < 0.05). Importantly, miR-23b has a targeted relationship with Smad3. Overexpression of miR- 23b induces autophagy by promoting the Smad3 expression, alleviates kidney damage in septic rats, and reduces inflammation and inactivates NF-κB signaling pathway.