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Photodynamic therapy (PDT) has emerged as a useful therapeutic modality not only in the treatment of cancer, but also in the treatment of atherosclerosis (AS). The majority of PDT studies have involved cancer therapy, whereas fewer studies have involved the treatment of AS. The molecular mechanisms underlying the role of PDT in the treatment of AS remain unclear. The purpose of this study was to determine the molecular mechanisms underlying the activity of PDT, using mesoporous-silica-coated upconversion fluorescent nanoparticles parceling Chlorin e6 (UCNPs-Ce6) in the induction of apoptosis in THP-1 macrophages.
The ability of UCNPs-Ce6-stimulated PDT to induce THP-1 macrophage apoptosis by facilitating the induction of ROS and regulation of mitochondrial permeability transition pore (MPTP) to depolarize mitochondrial membrane potential (MMP). Both Bax translocation and the release of cytochrome C were examined using immunofluorescence and western blotting.
The levels of ROS were significantly increased in the PDT group, resulting in both MPTP opening and MMP depolarization, which led to apoptosis. In addition, immunofluorescence and western blotting revealed that PDT induced both Bax translocation and the release of cytochrome C, as well as upregulation of cleaved caspase-9, cleaved caspase-3, and cleaved poly (ADP-ribose) polyserase.
UCNPs-Ce6-stimulated PDT induces apoptosis in THP-1 macrophages via ROS brusts. The proapoptotic factor Bax subsequently translocates from the cytosol to the mitochondria, resulting in the MPTP opening and cytochrome C release. This study demonstrated the great potential of UCNPs-Ce6 mediated PDT in the treatment of atherosclerosis.