4.2 Article

Protective effects of three remote ischemic conditioning procedures against renal ischemic/reperfusion injury in rat kidneys: a comparative study

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IRISH JOURNAL OF MEDICAL SCIENCE
卷 184, 期 3, 页码 647-653

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SPRINGER LONDON LTD
DOI: 10.1007/s11845-014-1227-8

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Remote ischemic perconditioning; Remote ischemic postconditioning; Kidney; Ischemic reperfusion injury

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Background Remote ischemic perconditioning (RIPerC), remote ischemic postconditioning (RIPostC), and remote ischemic perconditioning + postconditioning (RIPerC + RIPostC) protect against renal ischemia reperfusion injury (IRI). However, the most beneficial approach among these is not known. Aims To compare the protective effects and study the mechanisms of three different remote ischemic conditioning in preventing IRI in the rat kidney. Methods Fifty healthy adult male Sprague-Dawley rats were randomly assigned to five groups: sham, IRI, RIPerC, RIPostC, and RIPerC + RIPostC. Right nephrectomy was performed initially in all rats. IRI was induced by occluding the left renal artery for 60 min, followed by reperfusion for 24 h. RIPerC, RIPostC, and RIPerC + RIPostC were induced with 5-min ischemia/reperfusion (I/R) cycles using a tourniquet on the right hind limb. Results The IRI group showed significant serologic evidence of renal injury compared to the sham group (P < 0.05). The RIPerC, RIPostC, and RIperC + RIpostC groups displayed significantly lower levels of renal dysfunction than the IRI group (P < 0.05). Superoxide dismutase (SOD) levels were significantly lower in the IRI group than in the sham group (P = 0.003), but were significantly less depressed in the RIPerC, RIPostC, and RIperC + RIpostC groups (P < 0.05). The IRI group displayed more severe renal tubular injury than the RIPerC, RIPostC, and RIPerC + RIPostC groups (P < 0.05). Conclusion All three remote ischemic conditioning showed similar therapeutic potential for preventing renal IRI. The RIPerC + RIPostC protocol did not show an additive effect from the combination of preconditioning and postconditioning. The protective mechanism may be due to the stimulation of endogenous antioxidant activity by transient limb ischemia-reperfusion.

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