Cd Se/Zn S quantum dots induce photodynamic effects and cytotoxicity in pancreatic cancer cells

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:runzhong
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AIM: To investigate the photodynamic effect of Cd Se/Zn S 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 Cd Se/Zn S 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 Cd Se/Zn S QDs and illuminated.RESULTS: The CCK-8 assay results showed that both Cd Se/Zn S 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. Cd Se/Zn S 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 Cd Se/Zn S 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-photodynamictherapy-induced cell death.CONCLUSION: Cd Se/Zn S QDs can be used as a photosensitizer to inhibit SW1990 cell proliferation through ROS generation and apoptotic protein expression regulation. AIM: To investigate the photodynamic effect of Cd Se / Zn S 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 Cd Se / Zn S QDs (0 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 Cd Se / Zn S QDs and illuminated. RESULTS: The CCK-8 assay results showed both Cd Se / Zn S QDs with and without illumination suppressed SW1990 cell proliferation Ce Cd Se / Zn S 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 Cd Se / Zn S 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 Inhibition of ROS and apoptosis both attenuated QD-photodynamictherapy-induced cell death. CONCLUSION: Cd Se / Zn S QDs can be used as a photosensitizer to inhibit SW1990 cell proliferation through ROS generation and apoptotic protein expression regulation.
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