【摘要】：目的觀察碲化鎘量子點(diǎn)(CdTe QD)在體外對(duì)大鼠血管平滑肌細(xì)胞(VSMC)的損傷作用。方法CdTe QD(0.01~100 mg·L~(-1))與原代培養(yǎng)的大鼠胸/腹主動(dòng)脈平滑肌細(xì)胞共孵育24 h,MTT法檢測(cè)CdTe QD對(duì)細(xì)胞存活的抑制;鈣黃綠素乙酰甲酯(calcein-AM)熒光染色觀察CdTe QD對(duì)VSMC細(xì)胞活性的影響;DCFH-DA和JC-1染色、流式細(xì)胞術(shù)檢測(cè)CdTe QD作用后細(xì)胞內(nèi)活性氧(ROS)含量和線粒體膜電位的變化;流式細(xì)胞術(shù)檢測(cè)細(xì)胞凋亡;Western蛋白印跡法檢測(cè)BCL-2和BAX蛋白表達(dá)變化。結(jié)果 MTT結(jié)果顯示,CdTe QD 0.01~100 mg·L~(-1)作用VSMC細(xì)胞24 h,細(xì)胞存活率降低(P0.01),24 h IC_(50)值為25.60 mg·L~(-1)。Calcein-AM熒光檢測(cè)發(fā)現(xiàn),CdTe QD 0.1~25 mg·L~(-1)作用后,VSMC細(xì)胞活性下降。DCFH-DA染色結(jié)果顯示,CdTe QD 0.1~25 mg·L~(-1)使細(xì)胞內(nèi)ROS逐漸增加(P0.05,P0.01);JC-1染色結(jié)果表明,VSMC線粒體膜電位呈濃度依賴性降低(r=0.903,P0.01)。Western蛋白印跡結(jié)果表明,CdTe QD誘導(dǎo)抗凋亡蛋白BCL-2表達(dá)顯著降低(P0.01),促凋亡蛋白BAX表達(dá)顯著上升(P0.01);流式細(xì)胞術(shù)FITC-AnnexinⅤ染色結(jié)果顯示,CdTe QD 0.1~25 mg·L~(-1)作用24 h能顯著促進(jìn)VSMC細(xì)胞凋亡(P0.05,P0.01)。結(jié)論CdTe QD可誘導(dǎo)VSMC細(xì)胞凋亡,其機(jī)制可能與胞內(nèi)ROS含量上升和線粒體介導(dǎo)的凋亡通路激活相關(guān)。
[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，

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