摘要
以大鼠原代大脑皮质神经细胞为模型,以不同浓度(0、1、2.5、5、10μmol/L)的镉(Cd)染毒,免疫荧光观察自噬小体,Western-blotting检测细胞LC3蛋白表达水平,并检测了自噬特异性阻断剂羟氯喹(CQ)作用后细胞活性和酸性自噬泡的变化。结果显示,Cd可促使LC3-Ⅰ向LC3-Ⅱ转化,10μmol/L Cd作用4h,LC3-Ⅱ表达水平达到最高,神经细胞发生明显的聚点现象;CQ能明显降低自噬水平,抑制自噬,细胞活性明显降低。表明Cd能诱导大鼠原代大脑皮质神经细胞发生自噬,自噬在Cd引起的神经细胞损伤中起保护作用。
In order to investigate the role of autophagy in neurotoxicity induced by Cd,rat primary cerebral cortical neurons,were treated with different concentrations of cadmium（0,1,2.5,5,10 μmol/L）,autophago somes were observed by immunofluorescence,and the level of LC3 was detected by Western-blotting.The primary neurons were treated with CQ to examine cell viability and AVOs.The results showed that Cd can facilitate LC3-Ⅰturned into LC3-Ⅱ,the expressions of LC3 were up to maximum and LC3 puncta was observed apparently after treated with 10 μm cadmium for 4h.The autophagy inhibitor CQ with Cd reversed the number of AVOs and the level of cell viability.These findings suggest that cadmium can promote the autophagy of primary cultured cerebral cortical neurons and autophagy may play an important protect role in cadmium injury.
出处
《中国兽医学报》
CAS
CSCD
北大核心
2013年第9期1412-1416,共5页
Chinese Journal of Veterinary Science
基金
国家自然科学基金资助项目(31101866)
江苏高校优势学科建设工程资助项目
中国现代农业产业技术体系专项基金资助项目(CARS-40-30)
关键词
镉
自噬
大鼠
大脑皮质神经细胞
cadmium
autophagy
rat
cerebral cortical neurons
