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2011•Journal of Clinical Medicine in PracticeRequires access

The role of p38 MAPK in focal cerebral ischemia/reperfusion injury in rats

Hanrong Xu

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Abstract

Objective To study the mechanism of p38 MAPK after focal cerebral ischemia/reperfusion injury in rats.Methods Healthy male Sprague-Dawley rats were randomly divided into five groups: normal control group,sham group,ischemia/reperfusion group,SB202190 group and DMSO group.Except normal control group and sham group,rats′ cerebral ischemia/reperfusion model was established with suture method.In SB202190 group and DMSO group,SB202190(the specific inhibitor of p38 MAPK) and 1% of dimetyl sulphoxide(DMSO) were injected into the lateral ventricle respectively.The expression of Bcl-2 and Bax protein was studied and the behavioral score was recorded.Results ① Behavioral results: rats′ nerve function score of control group and sham group decreased after ischemia-reperfusion 24 h.Neurological function in SB202190 group was higher than in IR group,and there was statistical significance(P0.01).② Western blot test results: both Bcl-2 and Bax protein all express a few in normal control group and sham group,but there was no difference(P0.05).The expression of Bcl-2 protein decreased in IR group but there was no obvious statistical difference,Bax protein increased obviously at 24 h after ischemia/reperfusion(P0.05).Compared with IR group,the expression of bax protein in SB202190 group decreased,and there was obvious increases of Bcl-2 protein in SB202190 group(P0.05).Conclusion Inhibition of the p38 MAPK can protect neural function from being injured after focal cerebral ischemia/reperfusion injury in rats.

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Objective To study the mechanism of p38 MAPK after focal cerebral ischemia/reperfusion injury in rats.Methods Healthy male Sprague-Dawley rats were randomly divided into five groups: normal control group,sham group,ischemia/reperfusion group,SB202190 group and DMSO group.Except normal control group and sham group,rats′ cerebral ischemia/reperfusion model was established with suture method.In SB202190 group and DMSO group,SB202190(the specific inhibitor of p38 MAPK) and 1% of dimetyl sulphoxide(DMSO) were injected into the lateral ventricle respectively.The expression of Bcl-2 and Bax protein was studied and the behavioral score was recorded.Results ① Behavioral results: rats′ nerve function score of control group and sham group decreased after ischemia-reperfusion 24 h.Neurological function in SB202190 group was higher than in IR group,and there was statistical significance(P0.01).② Western blot test results: both Bcl-2 and Bax protein all express a few in normal control group and sham group,but there was no difference(P0.05).The expression of Bcl-2 protein decreased in IR group but there was no obvious statistical difference,Bax protein increased obviously at 24 h after ischemia/reperfusion(P0.05).Compared with IR group,the expression of bax protein in SB202190 group decreased,and there was obvious increases of Bcl-2 protein in SB202190 group(P0.05).Conclusion Inhibition of the p38 MAPK can protect neural function from being injured after focal cerebral ischemia/reperfusion injury in rats.

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Available abstract

Objective To study the mechanism of p38 MAPK after focal cerebral ischemia/reperfusion injury in rats.Methods Healthy male Sprague-Dawley rats were randomly divided into five groups: normal control group,sham group,ischemia/reperfusion group,SB202190 group and DMSO group.Except normal control group and sham group,rats′ cerebral ischemia/reperfusion model was established with suture method.In SB202190 group and DMSO group,SB202190(the specific inhibitor of p38 MAPK) and 1% of dimetyl sulphoxide(DMSO) were injected into the lateral ventricle respectively.The expression of Bcl-2 and Bax protein was studied and the behavioral score was recorded.Results ① Behavioral results: rats′ nerve function score of control group and sham group decreased after ischemia-reperfusion 24 h.Neurological function in SB202190 group was higher than in IR group,and there was statistical significance(P0.01).② Western blot test results: both Bcl-2 and Bax protein all express a few in normal control group and sham group,but there was no difference(P0.05).The expression of Bcl-2 protein decreased in IR group but there was no obvious statistical difference,Bax protein increased obviously at 24 h after ischemia/reperfusion(P0.05).Compared with IR group,the expression of bax protein in SB202190 group decreased,and there was obvious increases of Bcl-2 protein in SB202190 group(P0.05).Conclusion Inhibition of the p38 MAPK can protect neural function from being injured after focal cerebral ischemia/reperfusion injury in rats.

Key concepts: Medicine, Ischemia, p38 mitogen-activated protein kinases, Reperfusion injury, Western blot, Anesthesia, MAPK/ERK pathway, Immunohistochemistry

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