Renal ischaemia-reperfusion injury (IRI), as a common type of clinical acute kidney injury (AKI), causes injury to the kidney and can even result in acute renal failure (ARF). 1,2 Convincing evidence has revealed the molecular and pathological events in AKI. [3][4][5] Oxidative stress plays a vital role in renal IRI-induced cell apoptosis and is the result of the imbalance between oxidative and antioxidant systems. 6,7 The production of excessive ROS eventually cause membrane lipid peroxidation and oxidative damage to proteins and DNA and lead to apoptosis and necrosis. 8MicroRNAs (miRNAs), small noncoding RNAs (ncRNAs), can regulate gene expression by targeting corresponding mRNAs. In