Ischemic Preconditioning Promotes Autophagy and Alleviates Renal IschemiaReperfusion Injury

Abstract EN

Autophagy is important for cellular survival during renal ischemia/reperfusion (I/R) injury.

Ischemic preconditioning (IPC) has a strong renoprotective effect during renal I/R.

Our study here aimed to explore the effect of IPC on autophagy during renal I/R injury.

Rats were subjected to unilateral renal ischemia with or without prior IPC.

Hypoxia/reoxygenation (H/R) injury was induced in HK-2 cells with or without prior hypoxic preconditioning (HPC).

Autophagy and apoptosis were detected after reperfusion or reoxygenation for different time.

The results showed that the levels of LC3II, Beclin-1, SQSTM1/p62, and cleaved caspase-3 were altered in a time-dependent manner during renal I/R.

IPC further induced autophagy as indicated by increased levels of LC3II and Beclin-1, decreased level of SQSTM1/p62, and accumulation of autophagosomes compared to I/R groups at corresponding reperfusion time.

In addition, IPC reduced the expression of cleaved caspase-3 and alleviated renal cell injury, as evaluated by the levels of serum creatinine (Scr), neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1) in renal tissues.

In conclusion, autophagy and apoptosis are dynamically altered during renal I/R.

IPC protects against renal I/R injury and upregulates autophagic flux, thus increasing the possibility for a novel therapy to alleviate I/R-induced acute kidney injury (AKI).