Acute kidney injury (AKI) is a severe
kidney disease defined by partial or abrupt loss of renal function. Emerging evidence indicates that non-coding RNAs (ncRNAs), particularly long non-coding RNAs (lncRNAs), function as essential regulators in AKI development. Here we aimed to explore the underlying molecular mechanism of the
lncRNA H19/miR-130a axis for the regulation of
inflammation, proliferation, and apoptosis in kidney epithelial cells. Human renal proximal tubular cells (HK-2) were induced by
hypoxia/reoxygenation to replicate the AKI model in vitro.
After treatment, the effects of
LncRNA H19 and miR-130a on proliferation and apoptosis of HK-2 cells were investigated by
CCK-8 and flow cytometry. Meanwhile, the expressions of
LncRNA H19, miR-130a, and inflammatory
cytokines were detected by qRT-PCR, western blot, and ELISA assays. The results showed that downregulation of
LncRNA H19 could promote cell proliferation, inhibit cell apoptosis, and suppress multiple inflammatory
cytokine expressions in HK-2 cells by modulating the miR-130a/BCL2L11 pathway. Taken together, our findings indicated that
LncRNA H19 and miR-130a might represent novel therapeutic targets and early diagnostic
biomarkers for the treatment of AKI.