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目的:初步观察咪唑啉Ⅰ_2受体的高选择性配体2-(2-苯并呋喃基)-2-咪唑啉(2-BFI)对大鼠局灶性脑缺血再灌注损伤的影响。方法:建立SD大鼠大脑中动脉局灶性脑缺血模型。在脑缺血后即通过大鼠尾静脉给予生理盐水、2-BFI或咪唑克生。通过2,3,5-三苯基氯化四唑染色检测梗死体积并评价大鼠的神经功能缺损。通过免疫组化方法检测caspase-3蛋白和原位细胞凋亡法检测缺血半暗带中凋亡神经细胞数。结果:在局灶性脑缺血24h后,2-BFI和咪唑克生都能够显著提高神经功能评分。给予2-BFI或咪唑克生都可以显著降低梗死体积、减少caspase-3阳性细胞数(P<0.01)和凋亡细胞数(P<0.05)。结论:2-BFI和咪唑克生对局灶性脑缺血再灌注损伤大鼠有神经保护作用,为脑卒中的治疗提供了新的治疗方法。
OBJECTIVE: To observe the effect of 2- (2-benzofuranyl) -2-imidazoline (2-BFI), a highly selective ligand of imidazoline I 2 receptor, on focal cerebral ischemia-reperfusion injury in rats. Methods: The focal middle cerebral artery occlusion model of SD rats was established. After cerebral ischemia, rats were given physiological saline, 2-BFI or midazolam by caudal vein. Infarct volume was measured by 2,3,5-triphenyltetrazolium chloride staining and neurological deficits in rats were assessed. The number of apoptotic neurons in the ischemic penumbra was detected by immunohistochemistry and caspase-3 protein in situ. RESULTS: After 24 h of focal cerebral ischemia, 2-BFI and midazolam significantly increased neurological scores. Administration of 2-BFI or midazolam significantly reduced infarct volume and decreased the number of caspase-3 positive cells (P <0.01) and apoptotic cells (P <0.05). CONCLUSION: 2-BFI and midazolam have neuroprotective effects on focal cerebral ischemia-reperfusion injury in rats and provide a new therapeutic approach for the treatment of stroke.