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1.
Chinese Journal of Radiological Medicine and Protection ; (12): 136-138, 2009.
Article in Chinese | WPRIM | ID: wpr-395386

ABSTRACT

Objective To study the radiosensitizing effect of caffic acid phenethyl ester(CAPE)on human cervical cancer HeLa cells.Methods MTT assay was used to measure the relation between the inhibition effect and CAPE concentrations by CAPE with different concentrations on HeLa cells for 24 hours.HeLa cells were divided into the control and experimental groups,both of which were given 0,2,4,6 and 8 Gy of 60Co γ-irradiation,respectively.The cell clones were counted.Meanwhile HeLa cells were divided into the control,CAPE,irradiation and combination groups.Flow cytometric analysis was adopted to detect the changes of cell cycle distribution induced by CAPE.Results The inhibition rate of CAPE acting on Hela cells increased with concentrations(F=126.49~3654.88,P<0.01).HeLa cells cloning survival decreased with the increase of radiation dose(F=174.42~9422.81,P<0.01).At the game radiation dose,HeLa cells cloning survival was less in experimental group than conlrol group(F=120.14~251.91,P<0.01).The mean lethal dose(D0)(1.45 and 1.82 Gy)and the quasi-threshold dose(Dq)(1.89 and 3.21 Gy)of HeLa cells in experimental group decreased comparing with control group,SER was 1.26.Compared with the sole irradiation group,cells in G2/M phase of the CAPE group and the sole irradiation group increased(P<0.01)while the combination group decreased(P<0.01).Conclusions CAPE could increase the radiation sensitivity of HeLa cells by G2/M arrest and may be related to the inhibition of the sub-lethal damage repair.

2.
Chinese Journal of Radiological Medicine and Protection ; (12): 360-363, 2009.
Article in Chinese | WPRIM | ID: wpr-393493

ABSTRACT

Objective To investigate the radiosensitizing effects of dihydroartemisinin(DHA)on human HeLa cells of cervical cancer irradiated by X rays.Methods Cell growth kinetics was determined using MTF assay.Cell survival was analyzed by elonogenic assay.The change of cell cycle and apeptosis was measured by flow cytometry.Results Dihydroartemisinin inhibited the growth of HeLa cells of human cervical cancer and showed a dose-dependent and time-dependent manner.Dihydroartemisinin(20 μmol/L)showed the radiosensitizing effects on HeLa cells,and the sensitizing enhancement ratio(SER)was 1.47.Dihydroartemisinin abrogated radiation-induced G2 arrest of the tested HeLa cells,the G2 ratio of medicine + radiation group dechned from 73.58% to 48.31%.Dihydroartemisinin enhanced the apoptosis of HeLa cells by X-irradiation,the apoptosis rates of medicine + radiation group significantly increased from 29.46%,48.04%,70.21% to 45.79%,66.36% and 79.58%,respectively for 2,4 and 6 Gy.Conclusions Dihydroartemisinin could increase the radiesensitivity of HeLa cells of human cervical cancer.Abrogation of radiation-induced C2 arrest could be part of the mechanism.

3.
Korean Journal of Obstetrics and Gynecology ; : 725-731, 2003.
Article in Korean | WPRIM | ID: wpr-135319

ABSTRACT

OBJECTIVE: The cytotoxic and radiosensitizing effects of Taxol in uterine sarcoma cell lines were investigated. METHODS: Two uterine sarcoma cell lines with different Taxol responses were used, namely, Taxol- sensitive and MDR gene negative MES-SA, and Taxol-resistant and MDR gene positive MES-SA/MX2 cells. These cells were treated with Taxol, radiation, or both, and cytotoxicities were compared by XTT assay and TUNEL staining. The cytotoxic mechanism was also studied by flow cytometry and by RT-PCR of the MDR gene expression. RESULTS: In Taxol-sensitive MES-SA cell lines, Taxol showed highly cytotoxic activity than radiation or the Taxol-radiation combined treatment. On the contrary, in Taxol-resistant MDR positive MES-SA/MX2 cell lines, Taxol significantly increased the sensitivity to radiation therapy, and increased cytotoxicity and apoptosis. Flow cytometry showed that treatment with Taxol alone produced the highest rate of cell cycle shifting to the G0/G1 phase in the MES-SA cell line. However, in the MES-SA/MX2 cell line, Taxol only treatment did not show significant cell cycle shifting compared to the control group. However, in cases of combined Taxolradiation treatment, the rate of cell cycle shifting was higher than for radiation treatment only. CONCLUSION: Taxol has cytotoxic and radiosensitizing effects on uterine sarcoma cell lines.


Subject(s)
Apoptosis , Cell Cycle , Cell Line , Flow Cytometry , Genes, MDR , In Situ Nick-End Labeling , Paclitaxel , Radiation-Sensitizing Agents , Sarcoma
4.
Korean Journal of Obstetrics and Gynecology ; : 725-731, 2003.
Article in Korean | WPRIM | ID: wpr-135318

ABSTRACT

OBJECTIVE: The cytotoxic and radiosensitizing effects of Taxol in uterine sarcoma cell lines were investigated. METHODS: Two uterine sarcoma cell lines with different Taxol responses were used, namely, Taxol- sensitive and MDR gene negative MES-SA, and Taxol-resistant and MDR gene positive MES-SA/MX2 cells. These cells were treated with Taxol, radiation, or both, and cytotoxicities were compared by XTT assay and TUNEL staining. The cytotoxic mechanism was also studied by flow cytometry and by RT-PCR of the MDR gene expression. RESULTS: In Taxol-sensitive MES-SA cell lines, Taxol showed highly cytotoxic activity than radiation or the Taxol-radiation combined treatment. On the contrary, in Taxol-resistant MDR positive MES-SA/MX2 cell lines, Taxol significantly increased the sensitivity to radiation therapy, and increased cytotoxicity and apoptosis. Flow cytometry showed that treatment with Taxol alone produced the highest rate of cell cycle shifting to the G0/G1 phase in the MES-SA cell line. However, in the MES-SA/MX2 cell line, Taxol only treatment did not show significant cell cycle shifting compared to the control group. However, in cases of combined Taxolradiation treatment, the rate of cell cycle shifting was higher than for radiation treatment only. CONCLUSION: Taxol has cytotoxic and radiosensitizing effects on uterine sarcoma cell lines.


Subject(s)
Apoptosis , Cell Cycle , Cell Line , Flow Cytometry , Genes, MDR , In Situ Nick-End Labeling , Paclitaxel , Radiation-Sensitizing Agents , Sarcoma
5.
China Oncology ; (12)1998.
Article in Chinese | WPRIM | ID: wpr-535511

ABSTRACT

PURPOSETo evaluate the radiosensitizing effect of cisplatin combined with radiotherapy for esophageal carcinoma. METHODS From 1989 to 1990. 60 patients with esophageal were treated. It was divided into two groups. Radiotherapy group (R) and radiotherapy plus cisplatin (20mg iv. twice a week) (R + C). A total dose of 66-70 Gy/6-7 wk was used in (R) and (R+C) group. RESULTS The 1 year. 3 year. 5 year survival rats were R : R+C = 46. 7%、20%、10% : 60%、30%、23%. CONCLUSION This study may imply that rational administration of cisplatin in the radiotherapy could improve the radiotherapy result of the esophageal carcinoma.

6.
Academic Journal of Second Military Medical University ; (12)1982.
Article in Chinese | WPRIM | ID: wpr-548937

ABSTRACT

This paper compares the radiosensitizing effect of metronidazole(M) with that of its derivatives(CM)on sarcoma 180 (S180).After i.p injection S180 bearing mice were either irradiated with y-ray 17Gy or unirradiated under aerated or tumor acute local hypoxic conditions.Results indicate that under hypoxic condition tumor growth Was inhibited within 10 d after a single i.p injection of drugs, but under aerated condition inhibition of tumor growth did not occur.CM was found to be stronger than M in tumor inhibiting effect.After aerated irradiation the drug groups demonstrated an apparent slowing down of tumor growth.But the difference between groups was not obvious.Hypoxic irradiation produced a very strong inhibiting effect in the drug groups.CM, especially when it was chelated with Ca++to form CMCa, was strongest in tumor growth inhibition.Its tumor inhibiting ratio was 77.4%, enhancement ratio(ER)2.46 and sensitizing enhancement ratio(SER)1.89.Its tumor inhibiting effect was stronger than irradiation without drug administration and irradiation after the administration of M.Its radiossnsitizng effect was found to be twice stronger than that of the original compound(M), but its toxic side effect was slighter than M.

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