부산대학교 도서관

Purpose: Acute kidney injury (AKI) is a serious complication of sepsis and is characterized by inflammatory response. MicroRNA-210 host gene (MIR210HG) is upregulated in human proximal tubular epithelial cells under treatment of inflammatory cytokines. This study aimed to explore the role of MIR210HG in sepsis-induced AKI. Materials and Methods: Cell viability was detected by a cell counting kit 8 assay. The levels of proinflammatory cytokines weredetected by enzyme-linked immunosorbent assay kits. The protein levels of p65, IκBα, and p-IκBα were examined by western blotanalysis. The nuclear translocation of nuclear factor kappa B (NF-κB) was detected by immunofluorescence assay. The histologicalchanges of kidneys were analyzed by hematoxylin and eosin staining assay. Results: Lipopolysaccharide (LPS) treatment significantly inhibited cell viability and increased productions of proinflammatorycytokines in proximal tubular epithelial cells (HKC-8). Additionally, MIR210HG levels in HKC-8 cells were increased by LPS treatment. MIR210HG silencing inhibited the LPS-induced cell inflammatory response. MIR210HG activated the NF-κB signalingpathway by promoting the phosphorylation of IκBα and nuclear translocation of p65. Rescue assays revealed that the MIR210HGinducedincrease of cytokines levels and decline of cell viability were rescued by QNZ treatment. Knockdown of MIR210HG decreasedblood urea nitrogen, serum creatinine, and proinflammatory cytokine levels in AKI rats. Moreover, the knockdown ofMIR210HG protected against AKI-induced histological changes of kidneys in rats. Conclusion: MIR210HG promotes sepsis-induced inflammatory response of HKC-8 cells by activating the NF-κB signaling pathway. This novel discovery may be helpful for the improvement of sepsis-induced AKI.