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CdSe/ZnS quantum dots induce photodynamic effects and cytotoxicity in pancreatic cancer cells

机译:CdSe / ZnS量子点在胰腺癌细胞中诱导光动力效应和细胞毒性

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摘要

AIM: To investigate the photodynamic effect of CdSe/ZnS quantum dots (QDs) on pancreatic cancer cells and elucidate the probable mechanisms.METHODS: The pancreatic cancer cell line SW1990 was treated with different concentrations of CdSe/ZnS QDs (0, 0.5, 1.0, 1.5, 2.0, 2.5 μmol/L), with or without illumination. The viability of SW1990 cells was tested using the Cell Counting Kit-8 (CCK-8) assay. The ultrastructural changes of SW1990 cells were observed by transmission electron microscopy. Apoptosis was detected by nuclear staining and flow cytometry (FCM). Reactive oxygen species (ROS) were measured by dichlorofluorescein diacetate via fluorescence microscopy. Expression of Bax, Bcl-2 and caspase-3 was measured by real-time polymerase chain reaction (PCR) and protein immunoblotting 24 h after SW1990 cells were treated with CdSe/ZnS QDs and illuminated.RESULTS: The CCK-8 assay results showed that both CdSe/ZnS QDs with and without illumination suppressed SW1990 cell proliferation. Cell viability was significantly lower when illuminated or with a longer incubation time and a higher light dose. CdSe/ZnS QDs with illumination caused ultrastructural changes in SW1990 cells, such as organelle degeneration and chromatin condensation and aggregation at the periphery of the nucleus. Fluorescence microscopy and FCM showed that CdSe/ZnS QDs (1.5 μmol/L) with illumination increased SW1990 cell apoptosis (53.2%) and ROS generation compared with no illumination. Real-time PCR showed that expression of Bax and caspase-3 was upregulated and Bcl-2 was downregulated. Immunoblotting results were consistent with real-time PCR results. Inhibition of ROS and apoptosis both attenuated QD-photodynamic-therapy-induced cell death.CONCLUSION: CdSe/ZnS QDs can be used as a photosensitizer to inhibit SW1990 cell proliferation through ROS generation and apoptotic protein expression regulation.
机译:目的:研究CdSe / ZnS量子点(QDs)对胰腺癌细胞的光动力作用,并阐明其可能的机制。方法:用不同浓度的CdSe / ZnS QDs处理胰腺癌细胞株SW1990(0,0.5,1.0 (1.5、2.0、2.5μmol/ L),有或没有照明。使用细胞计数试剂盒8(CCK-8)测定法测试SW1990细胞的生存能力。通过透射电镜观察SW1990细胞的超微结构变化。通过核染色和流式细胞术(FCM)检测凋亡。通过二氯荧光素二乙酸酯通过荧光显微镜法测量活性氧(ROS)。 CdSe / ZnS QDs处理SW1990细胞并照射24 h后,通过实时聚合酶链反应(PCR)和蛋白免疫印迹法检测Bax,Bcl-2和caspase-3的表达。结果:CCK-8检测结果表明CdSe / ZnS QDs在有和没有照明的情况下均能抑制SW1990细胞的增殖。光照或更长的孵育时间和更高的光剂量时,细胞活力显着降低。带有照明的CdSe / ZnS QD会引起SW1990细胞的超微结构变化,例如细胞器变性,染色质在核周围凝结和聚集。荧光显微镜和FCM显示,与未照明相比,有照明的CdSe / ZnS量子点(1.5μmol/ L)增加了SW1990细胞凋亡(53.2%)和ROS生成。实时PCR显示Bax和caspase-3的表达上调而Bcl-2的表达下调。免疫印迹结果与实时PCR结果一致。结论:CdSe / ZnS量子点可作为光敏剂,通过ROS的产生和凋亡蛋白的表达调控来抑制SW1990细胞的增殖。

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