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rhEPO on focal cerebral ischemia reperfusion injury mechanism
PAGE \* MERGEFORMAT 9
rhEPO on focal cerebral ischemia reperfusion injury mechanism
Of: Zhoutie Zhu Wang Wei Xiao-Ying Hu Chen Xue
[Abstract] Objective To observe the rhEPO on the hippocampus of ischemic stroke S100B protein expression at different time points the dynamic changes of rhEPO on focal cerebral ischemia reperfusion injury of the possible mechanisms. Methods 66 SD rats to establish focal cerebral ischemia-reperfusion (I / R model, were randomly divided into sham operation group (n = 6, cerebral I / R group (n = 30, rhEPO treatment group (n = 30, according to reperfusion time is divided into five sub- groups, each sub-group of six (6 h group, 12 h group, 1 d group, 3 d group, 7 d group, 2 h after ischemia and reperfusion. ischemia detected by immunohistochemistry at different time in each group head Ma ischemic core and the surrounding area S100B protein, in situ end labeling to detect the center of hippocampal ischemic neuronal apoptosis and the surrounding area. Results cerebral I / R injury group compared with sham control group, significantly increased the number of apoptotic (P lt;0.05, rhEPO treatment group and brain I / R group, the number of apoptotic cells was significantly reduced (P lt;0.05, immunohistochemistry showed, I / R group compared with sham control group, S100B protein expression significantly increased (P lt;0.05), rhEPO treatment group and brain I / R group, S100B protein expression was significantly decreased (P lt;0.05). Conclusion rhEPO by decreasing the expression of S100B protein, anti-apoptosis in focal ischemia I / R to produce a protective effect.
[Keywords:] EPO, cerebral ischemia, reperfusion injury, apoptosis
Recent studies have found that recombinant human erythropoietin (rhEPO on cerebral ischemia-reperfusion injury (I / R) have neuroprotective effects (1), S100B protein is a protein secreted by glial cells is a reflection of nerve cell damage markers , at home and abroad given the lack of rhEPO S100B p
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