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作 者:刘丹[1,2] 隋海娟[1] 张玲玲[1] 金英[1]
机构地区:[1]辽宁医学院药理学教研室,锦州121001 [2]瓦房店市中心医院,瓦房店116300
出 处:《中药药理与临床》2014年第4期81-84,共4页Pharmacology and Clinics of Chinese Materia Medica
摘 要: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。To study the protective mechanism of Cocoomyxa glocobotrydifomis on cerebral ischemia-reperfusion injury in rats. Meth- ods: Focal middle cerebral artery occlusion (MCAO) model was made by suture-occluded method. The infarct volume, the extent of edema and the neurological deficit were determined by the TIC staining, dry-weightlessness and Longa's score, respectively. The hippocampal tissue mitochondria extracts were prepared for Western blotting of Bcl-2, Bax and active caspase-3. Results: Compare with the sham operation group, model group rats significantly increased infarct volume, the extent of edema, and aggravated the neurological deficit. Model group rats were significantly reduced the expression of Bcl-2, and increased the expression of Bax and active caspase-3 in the hippocampal tissue mito- chondria extracts. Compare with the model group, Cocoomyxa glocobotrydifomis (50, 100 mg/kg) group and the positive control group sig- nificantly reduced infarct volume, the extent of edema, and aggravated the neurological deficit, significantly increased the expression of Bcl- 2, and reduced the expression of Bax and active caspase-3 in the hippocampal tissue mitochondfia extracts. Conclusion: Kokkomikusan wa- ter extract prevented the cerebral tissues from the injury by cerebral ischemia-reperfusion by the inhibition of apoptosis.
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