Effect of the Protective Role of Long-Term Ischemic Preconditioning on Acute Renal Impairment Due to Re-Ischemic Resection Through TLR-4 and TNF-α Signaling Pathway in Rats

Acute Kidney Injury (AKI) is an inflammatory process in which multiple inflammatory factors are involved. Recently, one of the ways to alleviate inflammation in AKI is to apply pre-conditioned ischemic remote control (RIPerC). The aim of the present study was to determine and investigate the protective role of long-term ischemic preconditioning in acute injury of all ischemia due to resection through the TLR-4 and TNF-α signaling pathways in the rat.

The present experimental study was conducted in 2016 on 30 male rats of Sprag Dolly breed with a weight range of 250 to 280 grams. Ratings were divided into three equal groups of control, re-ischemic resection (I / R) and re-ischemic resection with long-term ischemic preconditioning (RIPerC) predisposition. In this study, I / R re-bleeding was observed with bilateral closure of the artery and renal vein for 45 minutes and 24 hours. The RIPerC model consisted of four five-minute cycles (two minutes for closing the left femoral artery and three minutes for re-bleeding) at the onset of ischemic-renal failure. At the end of the resuscitation period, urine, blood, and kidney tissue samples were collected for functional, structural, and molecular analysis. The collected data were analyzed using SPSS software.

Ischemia-reperfusion caused tissue damage and subsequently impaired renal function, which was demonstrated by a decrease in creatinine clearance and an increase in its relative sodium excretion. In addition, in the I/R group, mRNA level of TLR-4 and TNF-α in tissue increased, whereas RIPerC (in this group, during ischemia, ischemia, and reperfusion in the femoral artery was done) simultaneously with I/R improved kidney structure and function and decreased expression of TLR-4 and TNF-α.

RIPerC protected the kidney against ischemia-reperfusion-induced kidney injury and probably this protective effect was exerted by inhibition of TLR-4 signaling pathway in the kidney.