脑缺血模型大鼠海马CRF、PKC蛋白表达研究

目的： 观测脑缺血再灌模型大鼠海马神经细胞CRF、PKC蛋白表达变化。方法: 采用免疫组化技术检测脑缺血模型大鼠于再灌2 h、6 h、24 h时海马神经细胞CRF、PKC蛋白表达量，CRF拮抗剂对照。结果: (1)CRF：假手术组海马区可见少量阳性细胞；模型组见大量阳性细胞，着色深，随时间延长增多。拮抗剂组阳性表达较少，着色较浅。模型组和盐水组CRF蛋白阳性表达面积均显著高于假手术组和CRF拮抗剂组（P<0.01）。(2)PKC：假手术组海马区阳性表达颗粒少，模型组和盐水组见大量阳性表达颗粒，拮抗剂组阳性表达颗粒稀疏。模型组和盐水组CRF蛋白阳性表达面积均显著高于假手术组和CRF拮抗剂组（P<0.01）。结论: 脑缺血再灌诱导CRF、PKC蛋白高表达是导致海马神经细胞迟发性死亡的重要因素；CRF蛋白激活PKC蛋白表达可能是CRF诱导缺血后神经组织损伤的机制。

Expression of CRF and PKC proteins in hippocampus of rats with cerebral ischemia and reperfusion

AIM:To observe the expression of CRF and PKC in rats with cerebral ischemia. METHODS: Using immunohistochemistry technique we measured the expression quantitatively of CRF and PKC proteins in the hippocampus in rats induced by MCAO at 2 h, 6 h and 24 h after reperfusion, contrast to CRF antagonist. RESULTS: (1) CRF: there were lots of positive and deeper dyeing neurons in hippocampus in model group and normal saline group rats, while there were a few positive and lighter dyeing neurons in sham group and CRF antagonist group. The positive expression areas of CRF protein in hippocampus in model group and normal saline group were significantly bigger than those in sham group and CRF-antagonist group(P<0.01), respectively. (2) PKC:there were a great number of denser positive granules in hippocampus in model group and normal saline group rats, while there were a few of scattered positive granules in sham group and CRF antagonist group. The positive expression areas of CRF protein in hippocampus in model group and normal saline group were significantly bigger than that in sham group and CRF-antagonist group (P<0.01), respectively. CONCLUSION: The high expression of CRF and PKC induced by cerebral ischemia may be one important factors that resulted in the delayed neuronal death in hippocampus. The CRF protein activated PKC expression, indicating an important pathology mechanism of nerve tissue damage induced by CRF.