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目的:探讨胶球藻多糖(Cocoomyxa gloeobotrydifomis,CGD)对线栓法大鼠局灶性脑缺血再灌注损伤保护作用机制的研究。方法:线栓法制备局灶性脑缺血再灌注损伤大鼠模型,用Longa’s法、TTC染色法、干燥失重法评价大鼠神经功能状态、脑梗死面积及脑水肿程度;Western blot蛋白免疫印迹分析检测海马组织线粒体中Bcl-2、Bax及caspase-3的蛋白表达水平。结果:与假手术组相比,模型组大鼠神经功能症状、梗死面积及脑水肿程度明显增高,线粒体内Bcl-2的表达明显降低、而Bax及caspase-3的表达明显增加。与模型组相比,胶球藻多糖(50、100 mg/kg)组及尼莫地平(1 mg/kg)组明显减少MCAO再灌注后脑梗死面积、脑水肿程度及改善神经功能症状,线粒体内Bcl-2的表达明显增加、而Bax及caspase-3的表达明显降低。结论:胶球藻多糖对脑缺血再灌注损伤有明显保护作用,其可能的作用机制之一是抑制细胞凋亡。
Objective: To investigate the protective effect of Coco-molybdoterdis (CGD) on focal cerebral ischemia-reperfusion injury in rats subjected to thread-plug method. Methods: The rat model of focal cerebral ischemia-reperfusion injury was established by suture method. The neurological status, infarct size and brain edema were evaluated by Longa’s method, TTC staining and dry weight loss method. Western blot The protein levels of Bcl-2, Bax and caspase-3 in mitochondria of hippocampus were detected. Results: Compared with the sham operation group, the neurological deficits, infarct size and brain edema in model group were significantly increased, the expression of Bcl-2 in mitochondria was significantly decreased, while the expression of Bax and caspase-3 were significantly increased. Compared with model group, Cisplastic polysaccharide (50, 100 mg / kg) group and nimodipine (1 mg / kg) group significantly reduced cerebral infarction area, degree of cerebral edema and neurological function after reperfusion of MCAO, Bcl-2 expression was significantly increased, while the expression of Bax and caspase-3 was significantly reduced. CONCLUSION: Polysaccharide from Pistia chinensis has a significant protective effect on cerebral ischemia-reperfusion injury. One of the possible mechanisms is that it inhibits cell apoptosis.