摘要
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。
Aim： To primarily investigate the effect of 2-（2-benzofu-ranyl）-2-imidazoline（2-BFI, the highly selective ligands of 12 imidazoline receptor）, on rat focal cerebral ischemia-reperfusion injury in rats. Methods： Focal ischemia was induced by the suture occlusion of middle cerebral artery. Rats were treated with vehicle, 2-BFI or idazoxan immediately after focal ischemia via vena caudalis. Infarct volume was assessed by 2,3,5- triphenyltrazolium chloride（TrC） staining and neurobehavioral deficits were monitored. The number of apoptosis in the penumbra after ischemia was determined by immunostaining using anti-cleaved caspase-3 antibody and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling（TUNEL）. Results： Both 2-BFI and idazoxan significantly improved the neurological score compared with vehicle at 24 hours after focal ischemia reperfusion injury. Treatment with 2-BFI or idazoxan also significantly reduced infarct volume and the number of both caspase-3- and the TUNEL-positive cells in the penumbra compared with vehicle-treated rats （P〈0.01 and P〈0.05, respectively）. Conclusion： The results suggested the neuroprotective role of 2-BFI and idazoxan in focal cerebral ischemia reperfusion injury in rats, and may therefore represent useful targets for the developing new treatments for stroke.
出处
《中国临床神经科学》
2009年第6期580-584,621,共6页
Chinese Journal of Clinical Neurosciences
