碲化镉量子点对血管平滑肌细胞的损伤作用
发布时间：2018-08-21 09:02
【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(P0.01),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(P0.05,P0.01);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,P0.01)。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(P0.01),促凋亡蛋白BAX表达显著上升(P0.01);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(P0.05,P0.01)。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。
[Abstract]:Objective to observe the effect of cadmium telluride quantum dot (CdTe QD) on (VSMC) of rat vascular smooth muscle cells (VSMCs) in vitro. Methods the inhibition of CdTe QD on cell survival was detected by CdTe QD (0.01U 100mg L ~ (-1) co-incubation with primary cultured rat thoracic / abdominal aorta smooth muscle cells for 24 h, and the effect of CdTe QD on VSMC cell activity was observed by calcein-AM fluorescence staining. The changes of reactive oxygen species (ROS) content and mitochondrial membrane potential were detected by flow cytometry, and the expression of BCL-2 and BAX protein were detected by flow cytometry and Western blot. Results the results of MTT showed that the survival rate of VSMC cells decreased (P0.01) and the IC50 value was 25.60 mg / L ~ (-1). Calcein-AM fluorescence assay showed that the activity of VSMC cells was decreased after treated with 100mg L ~ (-1) of 100mg / L ~ (-1) of QD. DCFH-DA staining showed that CDTe QD _ (0.1) (25 mg / L ~ (-1) induced the cell viability of VSMC cells by 25 mg / L ~ (-1). The results of ROS staining showed that the cell viability was reduced by 25 mg / L ~ (-1) of CdTe QD (0.1 mg / L ~ (-1). The results of JC-1 staining showed that the mitochondrial membrane potential of VSMC decreased in a dose-dependent manner (r = 0.903, P 0.01). Western blot showed that the expression of anti-apoptotic protein BCL-2 was significantly decreased (P0.01), and the expression of pro-apoptotic protein BAX was significantly increased (P0.01), and that of flow cytometry FITC-Annexin was significantly increased (P0.01). The results of 鈪，
本文编号：2195224
[Abstract]:Objective to observe the effect of cadmium telluride quantum dot (CdTe QD) on (VSMC) of rat vascular smooth muscle cells (VSMCs) in vitro. Methods the inhibition of CdTe QD on cell survival was detected by CdTe QD (0.01U 100mg L ~ (-1) co-incubation with primary cultured rat thoracic / abdominal aorta smooth muscle cells for 24 h, and the effect of CdTe QD on VSMC cell activity was observed by calcein-AM fluorescence staining. The changes of reactive oxygen species (ROS) content and mitochondrial membrane potential were detected by flow cytometry, and the expression of BCL-2 and BAX protein were detected by flow cytometry and Western blot. Results the results of MTT showed that the survival rate of VSMC cells decreased (P0.01) and the IC50 value was 25.60 mg / L ~ (-1). Calcein-AM fluorescence assay showed that the activity of VSMC cells was decreased after treated with 100mg L ~ (-1) of 100mg / L ~ (-1) of QD. DCFH-DA staining showed that CDTe QD _ (0.1) (25 mg / L ~ (-1) induced the cell viability of VSMC cells by 25 mg / L ~ (-1). The results of ROS staining showed that the cell viability was reduced by 25 mg / L ~ (-1) of CdTe QD (0.1 mg / L ~ (-1). The results of JC-1 staining showed that the mitochondrial membrane potential of VSMC decreased in a dose-dependent manner (r = 0.903, P 0.01). Western blot showed that the expression of anti-apoptotic protein BCL-2 was significantly decreased (P0.01), and the expression of pro-apoptotic protein BAX was significantly increased (P0.01), and that of flow cytometry FITC-Annexin was significantly increased (P0.01). The results of 鈪，
本文编号：2195224
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