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| Modulation of protein kinase during ischemia/reperfusion brain injury |
| XU Zhong1, HE Xiaofei1, XU Kai1, XU Ruxiang2 |
1.Department of Neurosurgery, Hospital of Jiangsu Provincial Corps, Chinese People’s Armed Police Force, Yangzhou 225003, China;
2.Department of Neurosurgery, the Army General Hospital, Beijing 100700, China |
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Abstract Objective To explore the modulation of protein kinase during ischemia/reperfusion brain injury.Methods Primary hippocampal cultures were prepared from day-18 SD rat embryos. Hippocampal neurons were dissociated by incubation in typsin and purified with arabinosylcytosin (Ara-c), which could inhibit the proliferation of neuroglia. The postischemia time was simplified to 30 min and 60min. Changes of PKC activity in plasma and membrane were assessed by phosphoryl transfer pieces and the expression of PKCα protein was measured by Western blot.Results The activities of cytosolic PKC of the control group, ischemia 30 min group and ischemia 60 min group were (6.24±0.27) pmol/(min·mg), (3.26±0.21) pmol/(min·mg) and (3.05±0.17) pmol/(min·mg)respectively, while the activities of membrane PKC were (2.63±0.13) pmol/(min·mg), (8.85±0.32) pmol/(min·mg)and(10.63±0.35) pmol/(min·mg)respectively. After ischemia/reperfusion brain injury , the activities of cytosolic PKC were (0.97±0.19) pmol/(min·mg)and (0.82±0.16) pmol/(min·mg)respectively, while the activities of membrane PKC were (12.38±0.39) pmol/(min·mg)and (12.66±0.99) pmol/(min·mg)respectively. Ischemia and reperfusion injury significantly increased the activity of membrane PKC and decreased that of cytosolic PKC. These changes became more significant with the extension of ischmia duration. Similar results were also observed in the expression of PKCα protein.Conclusions Ischemia reperfusion injury of rats’ hippocampal neurons results in translocational activation of PKC, especially PKCα, and the activation might damage the neurons by promoting calcium overload.
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Received: 06 August 2017
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2018, Vol. 29 
