Nitric oxide-mediated activity in anti-cancer photodynamic therapy.

摘要: Cell recurrence in cancer photodynamic therapy (PDT) is an important issue that poorly understood. It becoming clear nitric oxide (NO) a modulator of PDT. By acting on the NF-κB/Snail/RKIP survival/anti-apoptotic loop, NO can either stimulate or inhibit apoptosis. We found pheophorbide a/PDT (Pba/PDT) induces release B78-H1 murine amelanotic melanoma cells concentration-dependent manner. Low-dose PDT low levels by stimulating anti-apoptotic nature above whereas high-dose stimulates high inhibiting loop and activating When are treated with low-dose Pba/PDT DETA/NO, NO-donor, intracellular increases cell growth inhibited according to scratch-wound clonogenic assays. Western blot analyses showed combined treatment reduces expression NF-κB Snail gene products pro-apoptotic RKIP product. The effect Pba DETA/NO was also tested C57BL/6 mice bearing syngeneic melanoma. used pegylated (mPEG-Pba) due its better pharmacokinetics compared free Pba. mPEG-Pba (30 mg/Kg) (0.4 were i.p. injected as single molecule combination. After photoactivation at 660 nM (fluence 193 J/cm(2)), delays tumor more efficiently than each individual (p<0.05). Taken together, our results efficacy strengthened when photosensitizer combination donor.