Remote ischemic per-conditioning protects against renal ischemia-reperfusion injury via suppressing gene expression of TLR4 and TNF-α in rat model.

BACKGROUND: The pathogenesis of renal ischemic reperfusion injury (IRI) involves both inflammatory processes and oxidative stress in the kidney. This study determined whether remote ischemic per-conditioning (RIPerC) is mediated by toll-like receptor 4 (TLR4) signaling pathway in rats.

MATERIALS AND METHODS: Renal I/R injury was induced by occluding renal arteries for 45 min followed by 24 h reperfusion. RIPerC included four cycles of 2 minutes ischemia of left femoral artery followed by 3 minutes reperfusion performed at the start of renal ischemia. Rats were grouped into sham, I/R, and RIPerC. At the ending of reperfusion period, urine, blood and tissue samples were gathered.

RESULTS: I/R created kidney dysfunction, as ascertained by significant decrease in creatinine clearance, and significant increase in sodium fractional excretion. This was occurred with a decrease in the activities of gluthatione peroxidase, catalase and superoxidae dismutase with an increment in malondialdehyde levels, mRNA expression levels of Toll-like receptor 4 (TLR4) and tumor necrosis factor-alpha (TNF-α) and histological damages in renal tissues. RIPerC treatment diminished all these changes.

CONCLUSION: This study demonstrated that RIPerC has protective effects on the kidney after renal I/R, which might be related with inhibition of TLR4 signaling pathway and augmentation of anti-oxidant systems.