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作 者:谭峰[1] 王健[1] 陈晶[1] 顾勇[2] 詹杰[1] 顾民华[2] 谭玖清[1] 梁艳桂[1]
机构地区:[1]广东省佛山市中医院,广东佛山528000 [2]南方医科大学南方医院,广东广州510515
出 处:《广州中医药大学学报》2017年第1期59-63,共5页Journal of Guangzhou University of Traditional Chinese Medicine
基 金:国家自然科学基金课题资助项目(编号:81473470,81072947);广东省自然科学基金重点项目(编号:8152800007000001,2014A030311033)
摘 要:【目的】探讨电针对大脑中动脉闭塞(MCAO)缺血再灌注(I/R)大鼠神经功能的影响及潜在机制,为应用电针治疗急性脑梗死提供实验依据。【方法】将54只雄性SPF级SD大鼠采用线栓法复制MCAO模型,按照随机数字表法分为假手术组、脑梗死组、电针组,每组18只大鼠。假手术组仅做手术创伤,脑梗死组不予任何干预,电针组予电针针刺百会穴、大椎穴,每天1次,每次30 min。各时间点(第1、7、14天)采用神经功能缺损评分量表评定神经功能,蛋白免疫印迹法(Western blot)检测病灶侧海马区勿动蛋白-A(Nogo-A)、Ras同源基因家族成员A(RhoA)、溶血磷脂酸(LPA)蛋白的表达。【结果】第1、7、14天脑梗死组神经功能缺损积分、海马区Nogo-A及LPA蛋白的表达均显著高于假手术组(P<0.05),第7、14天脑梗死组病灶侧海马区RhoA蛋白的表达显著高于假手术组(P<0.05);电针组第1、7、14天神经功能缺损积分、病灶侧海马区RhoA、Nogo-A及LPA蛋白的表达均显著低于同时间点脑梗死组(P<0.05)。【结论】电针可改善大鼠脑梗死后神经功能,其机制可能与电针抑制大鼠海马区RhoA通路相关蛋白的表达密切相关。Objective To investigate the effect of electroacupuncture(EA) on neurological function of rats with ischemia- reperfusion(I/R) induced by middle cerebral artery occlusion(MCAO) and to explore its possible mechanisms, as so to provide the proof for the treatment of acute cerebral infarction(ACI) with EA.Methods MCAO model was established by thread ligation method. A total of fifty-four male SPF SD rats were divided into sham operation group, model group and electroacupuncture(EA) group according to random number table, 18 rats in each group. The rats in the sham operation group was only given surgical trauma,model group had no treatment, and EA group received EA at acupoints of Baihui and Dazhui, once a day,lasting for 30 minutes each time. On experiment day 1,7,14,neurological function of the rats was tested by neurological function defect scale,the expression levels of Neurite outgrowth inhibitor-A(Nogo-A),Ras homolog gene family member A(RhoA),lysophosphatidic acid(LPA) in the hippocampus were detected by Western blotting method. Results The neurological function deficit scores and the expression levels of Nogo-A and LPA protein in hippocampal tissue in the model group were higher than those in the sham operation group on day1,7 and 14(P 0.05). The expression level of RhoA in the hippocampus was increased significantly in model group compared with that in sham operation group(P 0.05)on day 7 and 14. The neurological deficit scores and the expression levels of Nogo-A, LPA and RhoA in hippocampal tissue of EA group were lower than those in the model group on day 1,7 and 14(P 0.05). Conclusion EA can improve the nerve function of rats with cerebral infarction, and its mechanism may have correlation with EA in the inhibiting the expression of proteins related with RhoA signaling pathway in the hippocampus.
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