镉对大鼠大脑皮质神经细胞的氧化损伤及N-乙酰半胱氨酸的保护效应  

Cadmium-induced lipid peroxidation and protective effect of N-acetyl cysteine in cerebral cortical neurons of rats

作　　者：袁燕[1] 刘学忠[1] 卞建春 张英[1] 孙娅[1] 柴文娴[1] 闫汶[1] 刘宗平[1] 

机构地区：[1]扬州大学兽医学院,江苏扬州225009

出　　处：《中国兽医学报》2011年第3期391-393,401,共4页Chinese Journal of Veterinary Science

基　　金：江苏省高校"青蓝工程"中青年学术带头人培养对象资助项目(2006);江苏省自然科学基金资助项目(BK2008214)

摘　　要：为研究镉对新生大鼠原代大脑皮质神经细胞的脂质过氧化损伤及N-乙酰半胱氨酸(N-acetyl cysteine,NAC)的保护效应,对神经细胞用不同浓度(0、5、10、20μmol/L)醋酸镉染毒和NAC(100μmol/L)进行保护,检测细胞内活性氧(ROS)水平、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性及丙二醛(MDA)含量。结果表明,与对照组比较,染毒组细胞内ROS水平、MDA含量和CAT活性极显著升高(P<0.01),GSH-Px活性降低,20μmol/L组出现显著差异(P<0.05);NAC保护组与相应染毒组比较,ROS水平、MDA含量和CAT活性呈不同程度降低,部分组间出现显著差异(P<0.05);说明镉有促进神经细胞脂质过氧化的作用,NAC可提高神经细胞的抗氧化能力,对镉暴露所致的脂质过氧化损伤有一定的保护作用。To investigate the mechanisms of lipid peroxidation induced by cadmium and protective effect of N-acetyl cysteine（NAC） on primary cerebral cortical neurons of neonatal SD rats,the neurons were exposured to cadmium at different concentrations（0,5,10,20μmol/L） and/or NAC（100μmol/L）,respectively.Then,the level of reactive oxygen species（ROS）,the activities of glutathioneperoxidase（GSH-Px）,superoxide dismutase（SOD）,catalase （CAT） and the content of malondiadelhyde（MDA） in neurons were detected.In comparison with the control group, the level of ROS,the content of MDA and the activity of CAT increased significantly（P0.01）.Whereas the activity of GSH-Px decreased and significance（P0.05） was found in 20μmol/L group.Compared to the poisoning groups,ROS level of NAC protective groups together with CAT activities and MDA contents decreased with significant difference in partial groups（P0.05）.The results indicated that cadmium could promote lipid peroxidation in cortical neurons from neonatal SD rats,NAC could increase antioxidant effects and reduce lipid peroxidation caused by cadmium.

关 键 词：镉 大鼠 大脑皮质神经细胞 N-乙酰半胱氨酸 脂质过氧化 

分 类 号：S859.8[农业科学—临床兽医学]