SUN Yi, GUO Xiaorui, GU Xiaojie, QI Feng, MENG Peisong. Effect and mechanism of palmatine hydrochloride mediated laser therapy on proliferation and apoptosis in oral squamous cell carcinoma CAL-17 cells[J]. ACADEMIC JOURNAL OF CHINESE PLA MEDICAL SCHOOL.
Citation: SUN Yi, GUO Xiaorui, GU Xiaojie, QI Feng, MENG Peisong. Effect and mechanism of palmatine hydrochloride mediated laser therapy on proliferation and apoptosis in oral squamous cell carcinoma CAL-17 cells[J]. ACADEMIC JOURNAL OF CHINESE PLA MEDICAL SCHOOL.

Effect and mechanism of palmatine hydrochloride mediated laser therapy on proliferation and apoptosis in oral squamous cell carcinoma CAL-17 cells

  •   Background  The available treatments for oral squamous cell carcinoma mainly include surgery, radiotherapy, chemotherapy and so on, but the overall prognosis is still not satisfactory. Photodynamic therapy has been widely used in the treatment of oral cancers by its own advantages in recent years, and photosensitizer is the most important point. Therefore, the selection of a safe and effective photosensitizer is the key to achieve good results of photodynamic therapy.
      Objective  To investigate the effects of Palmatine hydrochloride (PaH) combined laser on the growth and apoptosis of oral squamous cell carcinoma (OSCC) cell CAL-27 and its mechanism.
      Methods  CAL-27 cells were randomly divided into control group, PaH group, Laser group and PaH combined with Photodynamic therapy (PaH-PDT) group (PaH: 2 μM + Laser: 2.4 J/cm2). CCK-8 assay was used to detect the viability of cells. Flow cytometry was used to detect each cell cycle distribution and apoptosis rate. DCFH-DA probe was used to detect intracellular reactive oxygen species (ROS) generation, and western blot was used to detect the expression of cell cycle and apoptosis related proteins.
      Results  Compared with control group, PaH and laser alone had no significant effect on the growth of CAL-27 cells, while PaH-PDT significantly inhibited cell proliferation. When the laser intensity was 1.2 J/cm2, 1.8 J/cm2 and 2.4 J/cm2, the IC50 of PaH was 8.3 μmol/L, 4.1 μmol/L and 2.1 μmol/L, respectively. PaH-PDT increased the ratio of cells in the G2/M phase, down-regulated the expressions of Cyclin B1 and CDK1, and up-regulated the expressions of P21 and P27. After treated by PaH-PDT, the apoptosis rate increased from (3.4±0.7)% to (35.17±3.9)% (P<0.05). PaH-PDT induced intracellular ROS production, up-regulated the expression of P53 and Bax, and down-regulated Bcl-2. Reactive oxygen scavengers showed that NAC could significantly reverse the effect of PaH-PDT on apoptotic proteins.中文摘要中没看到这句
      Conclusion  aaPAH can be used as a new photosensitizing agent to mediate the photodynamic therapy to inhibit the proliferation of oral cancer cell CAL-27 and induce its apoptosis. The mechanism may be related to the G2/M phase arrest induced by PaH-PDT and ROS production involved in the regulation of apoptotic proteins.
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