镉致大鼠大脑皮质神经细胞凋亡的机理及N-乙酰半胱氨酸的保护作用  

Apoptosis mechanism of rat′s primary cultured cerebral cortical neurons induced by cadmium and protective effect of N-acetyl cysteine

作　　者：袁燕[1] 张英[1] 卞建春 刘学忠[1] 李丹[1] 孙娅[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》2010年第8期1107-1110,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：对神经细胞用不同浓度(0、5、10、20μmol/L)醋酸镉染毒和N-乙酰半胱氨酸(NAC)(100μmol/L)进行保护,通过流式细胞仪检测了细胞凋亡率、[Ca2+]i和活性氧(ROS)水平。结果表明,与对照组相比,各染毒组细胞凋亡率、细胞内[Ca2+]i和ROS水平明显升高,呈剂量-效应关系,除5μmol/L组ROS水平外,均差异极显著(P<0.01)。添加NAC组与相应染毒组比较,神经细胞凋亡率有降低趋势,但差异不显著(P>0.05);10、20μmol/L组细胞内[Ca2+]i和ROS水平显著降低(P<0.05或P<0.01)。表明镉可诱导神经细胞凋亡,其机理可能与细胞内Ca2+和ROS水平升高有关,NAC对其有一定的保护作用。To investigate the mechanisms of apoptosis induced by cadmium and protective effect of N-acctyl cysteine（NAC） on primary cerebral cortical neurons of neonatal SD rats,the neurons were exposured to cadmium at different concentrations（0,5,10,20 μmol/L） and NAC（100 μmol/L）.Then,the apoptosis rates,intracelluar Ca2＋ concentration i and reactive oxygen species（ROS） were detected by flow cytometry.In comparison with the control group,the results showed that the apoptosis rate,intracelluar Ca2＋ concentration i and ROS level （apart from 5 μmol/L group） were increased significantly（P0.01）,with the dose-effect relationship.Compared to the poisoning groups,apoptosis rate in the NAC protective groups was decreased without significant difference（P0.05）,Ca2＋ concentration and ROS level of 10 and 20 μmol/L group decreased significantly（P0.05 or P0.01）.It was concluded that cadmium can promote the apoptosis of neuron,intracellular Ca2＋ and ROS may participate in this process,NAC has some effective protection against cadmium.

关 键 词：镉 皮质神经元 细胞凋亡 细胞内Ca2+浓度 活性氧 N-乙酰半胱氨酸 

分 类 号：S859.8[农业科学—临床兽医学]