LAUSR

OBJECTIVE Sepsis refers to the systemic inflammatory response caused by infection. Acute kidney injury (AKI) in sepsis is very common, and there are many complicated mechanisms for the occurrence of septic AKI. This article aimed to study the role of miR-942-5p in inflammation and apoptosis of septic AKI and its potential mechanism. MATERIALS AND METHODS Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was performed to detect the expression of RNAs. The protein expression was detected using Western blot. The contents of inflammatory factors in the cell supernatant were detected using commercial enzyme-linked immunosorbent assay (ELISA) kits. Cell Counting Kit-8 (CCK-8) assay was utilized to compare the cell viability of each group. Terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining and flow cytometry were used to observe cell apoptosis. RESULTS MiR-942-5p expression was reduced in lipopolysaccharide (LPS)-treated HK-2 cells. MiR-942-5p mimic could observably increase miR-942-5p expression. The overexpression of miR-942-5p dramatically inhibits the expression of inflammatory factors and Bax, but increase Bcl-2 expression. MiR-942-5p overexpression greatly reversed the LPS-induced decrease in viability of HK-2 cells. In addition, we observed that LPS can markedly increase the number of apoptosis, while miR-942-5p mimic can reduce it. CONCLUSIONS Taken together, our results demonstrated that miR-942-5p expression was reduced in the LPS-treated HK-2 cells, and miR-942-5p overexpression can inhibit LPS-induced inflammation and apoptosis of HK-2 cells via targeting FOXO3.