Investigation of radiation sensitivity and mechanism on SHG44 cells of human glioma induced by dihydrodihydroartemisinin
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Investigation of radiation sensitivity and mechanism on SHG44 cells of human glioma induced by dihydrodihydroartemisinin
Journal of Radiation Research and Radiation ProcessingVol. 29, Issue 3, Pages: 163-168(2011)
作者机构:
1.苏州大学医学部放射医学与公共卫生学院放射生物教研室 苏州 215123
2.苏州市立医院东区 苏州 215001
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JIANG Qing, CAO Jianping, JI Rong, et al. Investigation of radiation sensitivity and mechanism on SHG44 cells of human glioma induced by dihydrodihydroartemisinin. [J]. Journal of Radiation Research and Radiation Processing 29(3):163-168(2011)
DOI:
JIANG Qing, CAO Jianping, JI Rong, et al. Investigation of radiation sensitivity and mechanism on SHG44 cells of human glioma induced by dihydrodihydroartemisinin. [J]. Journal of Radiation Research and Radiation Processing 29(3):163-168(2011)DOI:
Investigation of radiation sensitivity and mechanism on SHG44 cells of human glioma induced by dihydrodihydroartemisinin
The subject is to investigate the radiation sensitivity and it’s mechanism on SHG44 cells of human glioma induced by dihydroartemisinin. MTT assay was used to measure the inhibition effect, cloning survival assay was used to study the radiation sensitized effect and flow cytometry was adopted to detect the changes of cell cycle distribution meanwhile western blot was used to examine the expression of CyclinB1, Cdc2. The results showed that dihydroartemisinin inhibited the proliferation of SHG44 cells in dose-dependent and time-dependent manner. DHA(5μmol/L) had obvious radiation sensitivity effect on SHG44 cells and the sensitized enhancement rat(SER) was 1.42. Compared with the radiation group, the G,2, /M ratio decreased and the expression of CyclinB1 increased while the expression of Cdc2 didn’t change in the radiation plus drug group. It can be concluded that dihydroartemisinin has radiation sensitivity effect on SHG44 cell, which may be related to weakening of the function of G,2, checkpoint by increasing the expression of CyclinB1 and relieve from the cycle blockage of G,2,/M stage.