关键词: 活性氧, 膜电位, 线粒体, 细胞凋亡, 丝裂原激活蛋白激酶, P38MAPK, 酞菁锌

Abstract: 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.

Key words: reactive oxygen species, membrane potential, mitochondrial, apoptosis, mitogen-activated protein kinases,
P38MAPK, TαPcZn