2013Zhongguo xiao-yiRequires access

Effect of urokallikrein on p38 MAPK signaling pathway of cerebral ischemia reperfusion injury model of rat

Jixing Chen

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Abstract

Objective To investigate the neuroprotective effect of urokallikrein on a cerebral ischemia-reperfusion injury model of rat.Methods Sixty male adult Sprague-Dawley rats were randomly assigned into three groups: a sham operation group(sham group),focal cerebral ischemia-reperfusion group(model group),and urokallikrein group.The middle cerebral artery occlusion reperfusion model was made by the suture method(ischemia for 2 hours,and reperfusion for 24 hours).After that,the rats were sacrificed by decapitation,the neurological function was evaluated,the pathological change was observed after HE staining,the expression of p38MAPK phosphorylation was detected by the immunohistochemical method,and apoptotic cells were measured by the TUNEL method 24 hours after ischemia-reperfusion injury.Results Compared with the sham group,the neurological function score was increased,the cell injury(HE staining) was more severe,the number of positive p-p38 cells and positive TUNEL cells were increased in rats after ischemia-reperfusion injury,the difference between the two groups was significant(P0.01).Compared with the model group,urokallikrein reduced the neurological function score,attenuated cell injury,and reduced the number of positive p-p38 cells and positive TUNEL cells.The difference between the two groups was significant(P0.01).Conclusions Urokallikrein has a neuroprotective effect on cerebral ischemia-reperfusion injury in rats,and its mechanism may be related to attenuating p38MAPK pathway and inhibiting neuronal apoptosis.

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Objective To investigate the neuroprotective effect of urokallikrein on a cerebral ischemia-reperfusion injury model of rat.Methods Sixty male adult Sprague-Dawley rats were randomly assigned into three groups: a sham operation group(sham group),focal cerebral ischemia-reperfusion group(model group),and urokallikrein group.The middle cerebral artery occlusion reperfusion model was made by the suture method(ischemia for 2 hours,and reperfusion for 24 hours).After that,the rats were sacrificed by decapitation,the neurological function was evaluated,the pathological change was observed after HE staining,the expression of p38MAPK phosphorylation was detected by the immunohistochemical method,and apoptotic cells were measured by the TUNEL method 24 hours after ischemia-reperfusion injury.Results Compared with the sham group,the neurological function score was increased,the cell injury(HE staining) was more severe,the number of positive p-p38 cells and positive TUNEL cells were increased in rats after ischemia-reperfusion injury,the difference between the two groups was significant(P0.01).Compared with the model group,urokallikrein reduced the neurological function score,attenuated cell injury,and reduced the number of positive p-p38 cells and positive TUNEL cells.The difference between the two groups was significant(P0.01).Conclusions Urokallikrein has a neuroprotective effect on cerebral ischemia-reperfusion injury in rats,and its mechanism may be related to attenuating p38MAPK pathway and inhibiting neuronal apoptosis.

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Available abstract

Objective To investigate the neuroprotective effect of urokallikrein on a cerebral ischemia-reperfusion injury model of rat.Methods Sixty male adult Sprague-Dawley rats were randomly assigned into three groups: a sham operation group(sham group),focal cerebral ischemia-reperfusion group(model group),and urokallikrein group.The middle cerebral artery occlusion reperfusion model was made by the suture method(ischemia for 2 hours,and reperfusion for 24 hours).After that,the rats were sacrificed by decapitation,the neurological function was evaluated,the pathological change was observed after HE staining,the expression of p38MAPK phosphorylation was detected by the immunohistochemical method,and apoptotic cells were measured by the TUNEL method 24 hours after ischemia-reperfusion injury.Results Compared with the sham group,the neurological function score was increased,the cell injury(HE staining) was more severe,the number of positive p-p38 cells and positive TUNEL cells were increased in rats after ischemia-reperfusion injury,the difference between the two groups was significant(P0.01).Compared with the model group,urokallikrein reduced the neurological function score,attenuated cell injury,and reduced the number of positive p-p38 cells and positive TUNEL cells.The difference between the two groups was significant(P0.01).Conclusions Urokallikrein has a neuroprotective effect on cerebral ischemia-reperfusion injury in rats,and its mechanism may be related to attenuating p38MAPK pathway and inhibiting neuronal apoptosis.

Key concepts: TUNEL assay, Ischemia, Neuroprotection, Medicine, Reperfusion injury, Apoptosis, Anesthesia, p38 mitogen-activated protein kinases

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