酞菁锌光动力治疗诱导大肠癌Lovo细胞产生活性氧.

Objective To investigate the P38MAPK-mediated mitochondrial damage induced by TαPcZn-PDT in Lovo cells. Methods Lovo cells were divided into control group, siRNA-negative group, siRNA-P38MAPK group, TαPcZn-PDT group and TαPcZn-PDT/siRNA-P38MAPK group. The cells in each group were treated and irradiated by red light for 10 minutes and then incubated for 3 hours. After incubation, RT-PCR and Western blot assay were used to detect the effect of p38MAPK silencing. The cell ROS levels were detected by DCFH-DA probe. JC-I/7-AAD double-labeled staining was used to detect changes of cell mitochondrial membrane potential (ΔΨm). Annexin V-FlOUS/7-AAD doublelabeled staining was used to detect the cell apoptotic rate. Results After siRNA interference, the protein expressions of P38MAPK mRNA significantly decreased. TαPcZn-PDT induced the increase of ROS, the depolarization of mitochondrial ΔΨm and the apoptotic rate. After siRNA silencing P38MAPK, the ROS was decreased, the number of depolarized cells was decreased and the apoptosis was weakened, which was induced by TαPcZn-PDT in Lovo cells. Conclusion That silencing of P38MAPK can significantly inhibit the production and release of ROS and decrease the depolarization of mitochondrial ΔΨm, thus attenuate the apoptosis induced by TαPcZn-PDT. [ABSTRACT FROM AUTHOR]