LAUSR

Renal ischemia‐reperfusion injury, a major cause of renal failure, always leads to acute kidney injury and kidney fibrosis. MicroRNAs (miRs) have been reported to be associated with renal ischemia‐reperfusion injury. miR‐194 was downregulated following renal ischemia‐reperfusion injury; however, the function and mechanism of miR‐194 in renal ischemia‐reperfusion injury have not yet been fully understood. In the present study, we constructed renal ischemia‐reperfusion injury model in vitro through treatment of human kidney proximal tubular epithelial cells HK‐2 by hypoxia/reperfusion (H/R). We observed that miR‐194 was decreased in H/R‐induced HK‐2 cells. miR‐194 mimic increased H/R‐induced HK‐2 cell survival, whereas miR‐194 inhibitor further strengthened H/R‐ inhibited HK‐2 cell survival. Also, we observed that miR‐194 overexpression suppressed oxidative stress markers, including malondialdehyde, glutathione, and secretion of pro‐inflammatory cytokines, including IL‐6, IL‐1β, and TNF‐α; however, miR‐194 inhibitor showed the reverse effects. Results from dual‐luciferase analysis confirmed that Ras homology enriched in brain (Rheb) was a direct target of miR‐194. Finally, we corroborated that miR‐194 affected cell growth, oxidative stress, and inflammation through targeting Rheb in H/R‐induced HK‐2 cells. In conclusion, our results suggested that miR‐194 protect against H/R‐induced injury in HK‐2 cells through direct targeting Rheb.