Abstract
The protective effects of ischemic postconditioning on renal ischemia/reperfusion injury in mice and the role of miR-126 and Nrf2 signaling pathway in the process were the focus of this study. Mice were classified into 5 groups: sham-operation, I/R6h, I/R24h, postconditioning (POC), and miR-126 agomir. Serum creatinine, renal histopathology changes, and oxidative stress were examined. The expression of miR-126 and Nrf2 were detected. We also treated NRK52E cells with hypoxia reoxygenation. The I/R group showed significant renal injury and increased generation of oxidative stress. However, the severity of renal injury and oxidative stress were markedly attenuated in the POC group. MiR-126 was downregulated, and Nrf2 was upregulated in NRK52E cells subjected to hypoxia/reoxygenation (H/R) and in mouse kidneys subjected to POC. Oxidative stress was higher and Nrf2 was lower in the mouse miR-126 agomir group; apoptosis were higher in H/R-treated NRK52E cells transfected with Nrf2 siRNA and lower in anti-miR-126. These findings demonstrate that after renal ischemic postconditioning, miR-126 inhibits oxidative stress by inducing Nrf2 and suppresses injury.
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