文献类型：期刊文献

中文题名：碲化镉量子点对血管平滑肌细胞的损伤作用

英文题名：CdTe quantum dots induced impairment in primary vascular smooth muscle cells

作者：严明[1];张云[2];刘珂舟[1];孙永红[3]

机构：[1]杭州电子科技大学生命信息与仪器工程学院;[2]绍兴文理学院基础医学院;[3]浙江大学生物医学工程与仪器科学学院浙江省心脑血管检测技术与药效评价重点实验室

年份：2017

卷号：31

期号：2

起止页码：165

中文期刊名：中国药理学与毒理学杂志

外文期刊名：Chinese Journal of Pharmacology and Toxicology

收录：CSTPCD、、北大核心2014、Scopus、CSCD2017_2018、北大核心、CSCD

基金：浙江省自然科学基金(LY15H180012);浙江省自然科学基金(LY17H060043);浙江省自然科学基金(LY14C100004);国家自然科学基金(31401008)~~

语种：中文

中文关键词：碲化镉量子点;血管平滑肌细胞;活性氧;线粒体膜电位;凋亡

外文关键词：CdTe quantum dot; vascular smooth muscle cells; reactive oxygen species; mitochondrial membrane potential; apoptosis

中文摘要：目的观察碲化镉量子点(CdTe QD)在体外对大鼠血管平滑肌细胞(VSMC)的损伤作用。方法CdTe QD(0.01~100 mg·L^(-1))与原代培养的大鼠胸/腹主动脉平滑肌细胞共孵育24 h,MTT法检测CdTe QD对细胞存活的抑制;钙黄绿素乙酰甲酯(calcein-AM)荧光染色观察CdTe QD对VSMC细胞活性的影响;DCFH-DA和JC-1染色、流式细胞术检测CdTe QD作用后细胞内活性氧(ROS)含量和线粒体膜电位的变化;流式细胞术检测细胞凋亡;Western蛋白印迹法检测BCL-2和BAX蛋白表达变化。结果 MTT结果显示,CdTe QD 0.01~100 mg·L^(-1)作用VSMC细胞24 h,细胞存活率降低(P<0.01),24 h IC_(50)值为25.60 mg·L^(-1)。Calcein-AM荧光检测发现,CdTe QD 0.1~25 mg·L^(-1)作用后,VSMC细胞活性下降。DCFH-DA染色结果显示,CdTe QD 0.1~25 mg·L^(-1)使细胞内ROS逐渐增加(P<0.05,P<0.01);JC-1染色结果表明,VSMC线粒体膜电位呈浓度依赖性降低(r=0.903,P<0.01)。Western蛋白印迹结果表明,CdTe QD诱导抗凋亡蛋白BCL-2表达显著降低(P<0.01),促凋亡蛋白BAX表达显著上升(P<0.01);流式细胞术FITC-AnnexinⅤ染色结果显示,CdTe QD 0.1~25 mg·L^(-1)作用24 h能显著促进VSMC细胞凋亡(P<0.05,P<0.01)。结论CdTe QD可诱导VSMC细胞凋亡,其机制可能与胞内ROS含量上升和线粒体介导的凋亡通路激活相关。

外文摘要：OBJECTIVE To study the effect of CdTe quantum dots（QD） induced injuries in vascular smooth muscle cells（VSMCs） and the potential mechanism.METHODS The rat thoracic/abdominal aorta VSMCs were treated with 0.01-100 mg·L^-1CdTe QD for 24 h.The cell survival of CdTe QD-treated VSMCs was detected with MTT assay.The cell viability of VSMCs was measured by calcein-AM staining.Then, the CdTe QD-treated VSMCs were labeled with DCFH-DA and JC-1 probes.The intracel ular ROS and mitochondrial membrane potential（MMP） were examined by flow cytometry.The cellular apoptosis in VSMCs was also examined in a flow cytometer after being labeled with FITC-Annexin Ⅴ.Finally, the level of mitochondrial apoptosis pathways proteins including BCL-2 and BAX was observed by Western blotting.RESULTS MTT data showed that CdTe QD（0.01-100 mg·L^-1）inhibited the cell survival（r=0.957, P〈0.01）, and that IC50 was 25.6 mg·L-1at 24 h.The results of calceinAM staining showed that the cell viability was gradually decreased.DCFH-DA staining results showed that 1-25 mg·L^-1CdTe QD induced an increase in intracellular ROS levels（P〈0.05, P〈0.01）.The results of JC-1 data showed a concentration-dependent disruption of MMP（r=0.903, P〈0.01）.Moreover, the results of Western blotting suggested that CdTe QD significantly increased the expression of BCL-2and decrease the expression of BAX in VSMCs（P〈0.01）.The flow cytometry results from FITC-Annexin Ⅴassay showed 0.1-25 mg·L^-1CdTe QD significantly increased the apoptosis of VSMCS.CONCULSION CdTe QD induces apoptotic cell death in VSMCs, which is possibly related to the up-regulation of intracellular ROS and activation of mitochondria-mediated apoptosis pathways.