2008Liaoning Yixueyuan xuebaoRequires access

Effect of Ischemic Postconditioning on the Renal Ischemia-reperfusion Injury in Rats

Huang Jian-hong

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Abstract

Objective To investigate the effect of ischemic postconditioning on the renal ischemia-reperfusion (I/R) injury and its mechanism.Methods The ischemia model with occlusion of left renal pedicel for 45 min in a right-nephrectomized rat was used in this experiment. Thirty male SD rats were anaesthetized 14 days after right nephrectomy. These rats were randomly divided into 3 groups (n=10 each): group I: sham operation (S), group II: I/R and group III: ischemic postconditioning (IPO). In IPO group, 45 min ischemia was followed by six 10 s episodes of ischemia at 10 s intervals for reperfusion. The rats were killed at 6 h of reperfusion. Blood urea nitrogen (BUN), creatinine (Cr) concentrations were measured. Kidneys were removed for determination of MDA content, SOD activity. The changes of renal tissue were detected by microscope. Renal apoptosis in the rats was assayed by flow cytometry.Results SOD activity was significantly lower whereas the serum BUN and Cr concentration, MDA content and the percentage of apoptotic renal cell were significantly higher in I/R group and IPO group than S group (P0.05). The serum BUN and Cr concentration, the MDA content and the percentage of apoptotic renal cell were significantly lower whereas the SOD activity was significantly higher in IPO group than in I/R group (P0.05). Microscopic examination showed that the renal I/R injury was significantly attenuated by ischemic postconditioning.Conclusions Ischemic postconditioning. attenuates the renal injury induced by I/R in rats, and the protective effect is associated with the inhibition of apoptosis in the renal tubular epithelial cell and enhancement of renal antioxidation.

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Objective To investigate the effect of ischemic postconditioning on the renal ischemia-reperfusion (I/R) injury and its mechanism.Methods The ischemia model with occlusion of left renal pedicel for 45 min in a right-nephrectomized rat was used in this experiment. Thirty male SD rats were anaesthetized 14 days after right nephrectomy. These rats were randomly divided into 3 groups (n=10 each): group I: sham operation (S), group II: I/R and group III: ischemic postconditioning (IPO). In IPO group, 45 min ischemia was followed by six 10 s episodes of ischemia at 10 s intervals for reperfusion. The rats were killed at 6 h of reperfusion. Blood urea nitrogen (BUN), creatinine (Cr) concentrations were measured. Kidneys were removed for determination of MDA content, SOD activity. The changes of renal tissue were detected by microscope. Renal apoptosis in the rats was assayed by flow cytometry.Results SOD activity was significantly lower whereas the serum BUN and Cr concentration, MDA content and the percentage of apoptotic renal cell were significantly higher in I/R group and IPO group than S group (P0.05). The serum BUN and Cr concentration, the MDA content and the percentage of apoptotic renal cell were significantly lower whereas the SOD activity was significantly higher in IPO group than in I/R group (P0.05). Microscopic examination showed that the renal I/R injury was significantly attenuated by ischemic postconditioning.Conclusions Ischemic postconditioning. attenuates the renal injury induced by I/R in rats, and the protective effect is associated with the inhibition of apoptosis in the renal tubular epithelial cell and enhancement of renal antioxidation.

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Available abstract

Objective To investigate the effect of ischemic postconditioning on the renal ischemia-reperfusion (I/R) injury and its mechanism.Methods The ischemia model with occlusion of left renal pedicel for 45 min in a right-nephrectomized rat was used in this experiment. Thirty male SD rats were anaesthetized 14 days after right nephrectomy. These rats were randomly divided into 3 groups (n=10 each): group I: sham operation (S), group II: I/R and group III: ischemic postconditioning (IPO). In IPO group, 45 min ischemia was followed by six 10 s episodes of ischemia at 10 s intervals for reperfusion. The rats were killed at 6 h of reperfusion. Blood urea nitrogen (BUN), creatinine (Cr) concentrations were measured. Kidneys were removed for determination of MDA content, SOD activity. The changes of renal tissue were detected by microscope. Renal apoptosis in the rats was assayed by flow cytometry.Results SOD activity was significantly lower whereas the serum BUN and Cr concentration, MDA content and the percentage of apoptotic renal cell were significantly higher in I/R group and IPO group than S group (P0.05). The serum BUN and Cr concentration, the MDA content and the percentage of apoptotic renal cell were significantly lower whereas the SOD activity was significantly higher in IPO group than in I/R group (P0.05). Microscopic examination showed that the renal I/R injury was significantly attenuated by ischemic postconditioning.Conclusions Ischemic postconditioning. attenuates the renal injury induced by I/R in rats, and the protective effect is associated with the inhibition of apoptosis in the renal tubular epithelial cell and enhancement of renal antioxidation.

Key concepts: Creatinine, Ischemia, Blood urea nitrogen, Medicine, Nephrectomy, Kidney, Renal ischemia, Reperfusion injury

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