MicroRNA-30b promotes lipopolysaccharide-induced inflammatory injury and alleviates autophagy through JNK and NF-κB pathways in HK-2 cells.

BACKGROUND: Acute kidney injury (AKI) is an abrupt loss of kidney function. MicroRNA-30b (miR-30b) has been reported to be involved in the inflammatory reaction of a variety of diseases. However, the role of miR-30b in AKI remains unknown. In this research, we aimed to investigate the role of miR-30b in lipopolysaccharide (LPS)-induced kindey inflammatory injury in vitro and in vivo.

METHODS: In vitro, after miR-30b mimic/inhibitor transfection and/or LPS treatment, the viability, apoptosis, autophagy and inflammatory cytokines releases, as well as activation of c-Jun-N-terminal kinase (JNK) and nuclear factor-kappa B (NF-κB) pathways were detected by cell counting kit-8 (CCK-8) assay, flow cytometry, qRT-PCR, enzyme-linked immunosorbent assay (ELISA) and western blot, respectively. In vivo, after LPS treatment and/or anti-miR-30b administration, the levels of creatinine, the activities of alanine aminotransferase (ALT) and histologic scores, as well as concentrations of inflammatory cytokines were assessed by creatinine assay kit, ALT assay kit and ELISA, respectively.

RESULTS: LPS inhibited HK-2 cell viability and induced HK-2 cell apoptosis, autophagy and the releases of inflammatory cytokines. Overexpression of miR-30b promoted LPS-induced HK-2 cell viability inhibition, cell inflammatory cytokines releases, cell apoptosis induction and activation of JNK and NF-κB signaling pathways, but inhibited LPS-induced HK-2 cell autophagy. Suppression of miR-30b had opposite effects. Moreover, suppression of miR-30b alleviated the LPS-induced kidney injury in mice model by decreasing creatinine level, ALT activity and histologic scores, as well as concentrations of inflammatory cytokines.

CONCLUSION: miR-30b participated in the LPS-induced kindey inflammatory injury in vitro and in vivo.