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作 者:陈一[1] 朴浩哲[1] 姚冰[1] 孙佩欣[1] 张烨[1] 隋锐[1] 郭旭[1] 史记[1] 梁海洋[1] 赵丽宏
机构地区:[1]中国医科大学肿瘤医院,辽宁省肿瘤医院神经外科,沈阳110042 [2]丹东市人民医院神经内科,丹东118000
出 处:《解剖科学进展》2017年第1期68-70,共3页Progress of Anatomical Sciences
基 金:辽宁省博士启动基金计划(20131059)
摘 要:目的探讨脑室内低温对家兔大脑中动脉梗塞模型脑组织bcl-2与Bax表达的影响。方法选用4-6个月龄雄性家兔20只,随机分为对照组(37℃常温生理盐水)和低温组(22℃低温生理盐水),各10只。应用线栓法建立大脑中动脉闭塞(MCAO)模型,进行脑室内穿刺低温液体灌注亚低温干预,24h后,参照Zea Longa及Bederson检查法进行评分。免疫组织化学方法和Western Blot方法检测各组脑组织bcl-2与Bax的表达,TUNEL方法检测细胞凋亡。结果兔神经病学体征评分以及动物行为观察发现,低温组评分明显优于常温组,P<0.01。与对照组相比,常温组家兔脑组织的bcl-2表达显著升高,Bax的表达显著下降,P<0.01。低温组的TUNEL染色凋亡细胞数明显低于常温组,P<0.01。结论脑室内穿刺低温干预可能通过调节bcl-2与Bax的表达对急性脑梗塞家兔动物模型提供脑保护作用。Objective To explore the effects of mild hypothermia on the expressions of bcl-2 and Bax in brain tissues of rabbits after middle cerebral artery occlusion. Methods 20 rabbits were randomly divided into the control group (37 ~C normal temperature liquid, n=10) and the mild hypothermia group(22 ~C low temperature liquid, n=10) after middle cerebral artery oeclusion(MCAO). The middle cerebral artery occlusion model was made by intralumial thread approach, then we trickled the lateral ventricle continuously with low temperature liquids to the mild hypothermia group and normal temperature liquid to the control group, and the pathological score was determined refer to ZeaLonga and Bederson examination after 24 hours. The expressions of bcl-2 and Bax were detected by immunochemistry and western blot methods, apoptosis was detected by TUNEL assay. Results From animal behavior, we observed the pathological score was significantly in mild hypothermia group than in control group, P〈0.01. Compared with control group,the expression of bcl- 2 was increased,and the expression of Bax was decreased significantly in brain tissues of rabbits in mild hypothermia group, P〈0.01. The number of the apoptosis cells in the brain tissues were much lower in mild hypothermia group than in control group, P〈0.01. Conclusion The way of continuous trickle oflowtemperature liquids might provide the protection of rabbits brain after middle cerebral artery occlusion by regulating the expressions of bcl-2 and Bax.
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