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作 者:刘庆杰[1] 王伟[2] 白宏英[3] LIU Qingjie1 ,WANG Wei2 ,BAI Hongying3(1 )Department of Neurology, the People's Hospital of Yongcheng City,Yongcheng 476600, China ; 2) Nanyang Medical College, Nanyang 473061, China ; 3) Department of Neurology, the Second Affiliated Hospital of Zhengzhou University, Zhengzhou 450014, Chin)
机构地区:[1]永城市人民医院神经内科,河南永城476600 [2]南阳医学高等专科学校,河南南阳473061 [3]郑州大学第二附属医院神经内科,河南郑州450014
出 处:《中国实用神经疾病杂志》2018年第4期357-360,共4页Chinese Journal of Practical Nervous Diseases
基 金:河南省医学教育研究课题;编号:Wjlx2016152
摘 要:目的研究硫辛酸对大鼠局灶性脑缺血再灌注损伤的保护作用,进一步探讨其机制。方法 54只雄性清洁SD大鼠按照随机原则平均分成3组:假手术组(18只)、脑缺血再灌注组(对照组18只)、脑缺血再灌注+硫辛酸治疗组(治疗组18只)。大鼠大脑中动脉局灶性缺血2 h(MCAO),再灌注24 h。治疗组在再灌注同时经颈外静脉给予硫辛酸20 mg/kg,假手术组和对照组给予相同体积的溶媒。采用TTC染色法检测大鼠脑组织梗死体积;采用RT-PCR法检测大鼠脑组织TNF-α的表达;采用TUNEL法检测大鼠脑组织凋亡细胞数。结果与假手术组相比,对照组和治疗组大鼠脑组织梗死体积,TNF-α的表达和凋亡细胞数均明显增加(均P<0.05)。与对照组相比,治疗组大鼠脑组织梗死体积,TNF-α的表达以及凋亡细胞数均明显减少(均P<0.05)。结论我们的研究结果表明,硫辛酸对大鼠脑缺血再灌注损伤具有保护作用,可能机制为减轻脑缺血再灌注引起的炎症反应和细胞凋亡。Objective To investigate the protective effect of lipoic acid on focal cerebral ischemia reperfusion-induced injury in rats and further exploring the underlying mechanisms. Methods Fifty-four male clean SD rats were divided into three groups by the random number method: sham operation group (SO group, n = 18), cerebral ischemia-reperfusion group (I/R group, n =18), cerebral ischemia-reperfusion group plus lipoic acid treatment group (treatment group,n = 18). Rats were subjected to 2h of tran- sient middle cerebral artery occlusion (MCAO), followed by 24h of reperfusion. Lipoic acid (20 mg/kg) was administered in 18 animals (treatment group) through the external jugular vein immediately after reperfusion. An equivalent volume of vehicle was administered to 36 animals (SO group and I/R group). The infarct volume of animals was determined by the 2,3,5-triphenyltet- razolium chloride staining. The expression level of TNF-α was detected by RT-PCR and the apoptotsis was detected by TUNEL method. Results Compared to SO group, cerebral infarction area, neuronal apoptosis and cerebral TNF-α production were enhanced significantly in I/R and treatment group. Compared to I/R,lipoie acid reduced cerebral infarction area, neuronal apoptosis and cerebral TNF-α production. Conclusion Our results suggested that lipoic acid has protective effects against cerebral I/R injury in rats,which may be attributed to attenuating inflammation and apoptosis induced by cerebral ischemia.
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