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目的:探讨巴曲酶对沙土鼠脑缺血再灌注神经元保护作用的可能机制。方法:蒙古沙土鼠63只分为巴曲酶组45只,假手术组9只及对照组9只。对照组及巴曲酶组鼠制作缺血再灌注模型,假手术组仅行手术操作,不行缺血处理。巴曲酶组于缺血再灌注前0、0.5、13、和6h时分别给予腹腔注射巴曲酶8 BU/kg,每个时间点9只。缺血再灌注96 h后3组鼠进行免疫组化SP法检测海马CA1区的Bcl-2、eNOS、VEGF及Akt蛋白的表达及电镜下神经元超微结构观察;并在光镜下计算海马CA1区的神经元阳性细胞数。结果:巴曲酶组使用巴曲酶后,Bcl-2e、NOS、VEGF及Akt蛋白表达明显增加,神经元阳性细胞数在各时间点与对照组比较差异均有显著性意义(P<0.01),而巴曲酶组各个时间点间比较差异无统计学意义;超微结构显示巴曲酶各时间点抗细胞凋亡明显。结论:巴曲酶具有明显的海马CA1区的神经元保护作用,其机制可能是通过其上调Bcl-2、eNOS、VEGF及Akt蛋白的表达。
Objective: To explore the possible mechanism of batroxobin on the neurons in gerbil cerebral ischemia-reperfusion injury. Methods: 63 Mongolian gerbils were divided into batroxobin group (n = 45), sham operation group (n = 9) and control group (n = 9). The control group and the batroxobin group mice were given ischemia-reperfusion model. The sham operation group was operated only without ischemia. Batroxobin group were given intraperitoneal injection of 8 BU / kg batroxobin at 0, 0.5, 13, and 6 h before reperfusion, respectively, 9 at each time point. The expression of Bcl-2, eNOS, VEGF and Akt protein in hippocampal CA1 region were detected by immunohistochemical SP method at 96 h after ischemia / reperfusion and the ultrastructure of neurons was observed under electron microscope. The hippocampus CA1 area neurons positive cells. Results: The batroxobin group showed a significant increase in the expression of Bcl-2e, NOS, VEGF and Akt after treatment with batroxobin. The number of neuronal positive cells at each time point was significantly different from that in the control group (P <0.01) , While Batroxobin group had no significant difference at all time points; ultrastructure showed that anti-apoptosis was obvious at all time points of Batroxobin. CONCLUSION: Batroxobin has neuroprotective effect in hippocampal CA1 region, which may be related to its up-regulation of Bcl-2, eNOS, VEGF and Akt protein expression.