作者: Qin Xue , Xiaobing Wang , Pan Wang , Kun Zhang , Quanhong Liu
DOI: 10.1016/J.PDPDT.2014.12.001
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摘要: Summary Background Photodynamic therapy (PDT) has been undergoing clinical evaluation for the treatment of colorectal cancer. But molecular mechanism photodynamic injury in human cancer cells still remains unclear. Methods Chlorin e6 (Ce6) was used to photosensitize SW620 cells. The inhibitory effect PDT evaluated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltertrazolium bromide tetrazolium) assay and colony forming assay. Apoptosis determined nuclear DAPI (4′-6-diamidino-2-phenylindole) staining Annexin V-PE/7-AAD Monodansylcadaverine (MDC) evaluate abundance autophagic vacuoles treated apoptosis autophagy associated proteins were analyzed western blotting. Moreover, we applied siRNA p38MAPK inhibitor SB203580 dissect its on cellular response Results Ce6 mediated (Ce6-PDT) induced apparent with dependent ROS (reactive oxygen species) generation. When inhibited or SB203580, a marked enhancement detected after PDT. 3-methyladenine/Bafilomycin A1 greatly aggravated photodamage Conclusion Ce6-PDT production activate probably prevent from photodamage. Inhibition activation accelerated cell apoptosis, meanwhile enhanced may act as cytoprotective process