DIOMED 630 PDF

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Int J Clin Exp Med. Published online Sep The apoptotic outcome was accompanied by concurrent generation of ROS. PDT is a light-based oncological and non-malignant diseases treatment modality, in which visible light is used to activate a photosensitizer, a light-absorbing molecule. Namely, the tumor-targeting photosensitizing molecule is administered followed by a light of a corresponding wavelength irradiation so as to induce the generation of reactive oxygen species ROS which was proven to be responsible for the DNA damage and cell death [ 1 ].

Dougherty etc has reported the significant clinical efficacy of PDT, which was later approved as the first drug-device combination by US Food and Drug Administration [ 2 , 3 ]. To date, various tumors including esophagus cancer [ 4 ], gastric cancer [ 5 ], skin caner [ 6 ], head and neck cancer [ 7 ], etc have been treated by PDT.

It has been established that PDT could induce apoptotic, necrotic and autophagy cell death. Wu etc showed that ALA-mediated PDT initiated apoptotic cell death via the up-regulation and activation of p38 mitogen activated protein kinase MAPK , the stress-activated c-jun N-terminal kinases JNK and ERK [ 8 ]; Mohamed etc demonstrated the results based on the cytoplasmic organelles and the intranuclear localization extensively enhanced the efficacy of PDT with appropriate photosensitizer and light dose and support the idea that PDT can contribute to elimination of malignant cells by inducing apoptosis, which is of physiological significance [ 9 ]; H Wang etc reported that DTPP showed an efficient growth inhibition of MCF-7 during PDT treatment [ 10 ].

Porfimer sodium Photofrin II is a photosensitizer which distributes selectively to tumor tissues, and causes tumor cell death by combination with light irradiation. Porfimer sodium is activated by laser irradiation at nm, which can reacts with tissue oxygen to produce highly reactive excited siglet oxygen 1O2 [ 11 ]. Moreover, photofrin-mediated PDT has been suggested to allow for preservation of function and structure of the larynx without systemic toxicity [ 17 ], to induce apoptosis and inhibit survival of human pancreatic cancer cells [ 18 ], to treat T1 and T2 oral squamous cell carcinoma [ 19 ].

However, the molecular mechanisms in esophageal cancer during PDT remain unclear. Materials and methods Ethics statement For tissue samples, written informed consent was obtained from patients. The procedures used in this study were approved by the Institutional Review Board of the Henan University of Science and Technology and was conformed to the Helsinki Declaration, and to local legislation. The details of the settings in the laser system as well as the optimal doses of photofrin and laser irradiation in vitro and in vivo were as described previously [ 21 , 22 ].

Images of cellular fluorescence were captured using MetaMorph software Molecular Devices, MDS Analytical Technologies and the average pixel intensities were determined using morphometric analysis. Cells were harvested at min after treatment with photofrin with or without subsequent irradiation.

Unstained cells were used as negative controls. Data was analyzed with FlowJo version7. MTT assay The viability of cells incubated with photofrin of different concentration and for different time were examined by MTT ,5-diphenyl tetrazolium bromide assay Sigma, USA as described previously [ 23 , 24 ]. All experiments were performed with five wells per experiment in triplicate. Soft agar colony-formation assays 2. Then, the gel was laser irradiated 24 h after the gel formation, and cells were allowed to grow for another 2 weeks.

Colonies were stained with 0. A , and the number and the size of colonies per high-power field were measured later. Differences in values were considered as significant if the P-value was less than 0. As shown in Figure 1 , when incubated for min, photofrin was incorporated in SHEE and SHEEC cells in a dose-dependent manner; when incubated at specific concentration of photofrin, photofrin uptake peaked at min.

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DIOMED 630 PDF

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Apoptotic effects of Photofrin-Diomed 630-PDT on SHEEC human esophageal squamous cancer cells

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