| Objectives:To study the anti-apoptotic mechanisms of heme oxygenase-1in aged rat ischemia/reperfusion injury (IRI) kidney.Methods:Twenty five month old male Wistar rats were randomly divided into control group, I/R model group, CoPP group, ZnPP group and CoPP+SB203580group. Twenty four hours after successful modeling, the kidney tissues were obtained. RT-PCR and Western blot were used to detect the expression of HO-1protein, and immunohistochemistry to detect the expression of Caspase-3, flow cytometry to detect renal cell apoptosis. Western blot to detect P38MAPK phosphorylation.Results:RT-PCR and Western blot results showed that there were the presence of HO-1mRNA and protein expression in normal renal tissue, and the expression of HO-1significantly was increased in I/R group. CoPP promoted the expression of HO-1, while ZnPP inhibited HO-1expression. Immunohistochemical results showed Caspase-3expression level was significantly elevated in I/R model group. Compared with the I/R model group, the expression level of Caspase-3was significantly lower in CoPP group, while significantly increased in ZnPP group and SB203580group. Results of flow cytometry showed cell apoptosis rate was increased in I/R model group. Compare with the I/R model group, cell apoptosis rate was decreased significantly in CoPP group, while increase in ZnPP group and SB203580group. Western blot results showed that p38MAPK phosphorylation level was significantly elevated in I/R model group. CoPP promoted p38MAPK phosphorylation, as well as the specific inhibitor of p38MAPK SB203580, HO-1inhibitor ZnPP inhibited p38MAPK phosphorylation.Conclusion:HO-1played a role on aged rat IRI kidney protection through its anti-apoptotic effect by increasing P38MAPK phosphorylation and inhibiting Caspase-3expression. |
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