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Effects of radiation from ~(188) Re on smooth muscle cell proliferation / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12)2000.
Article in Chinese | WPRIM | ID: wpr-518478
ABSTRACT

AIM:

Although endovascular radiotherapy inhibits neointimal hyperplasia, the exact alterations induced by ?-particles irradiation remain to be elucidated. The objective of this study was to investigate the ability and the cellular mechanism of local ?-particles emission from 188 Re to inhibit vascular smooth muscle cells (SMCs).

METHODS:

The SMCs in vitro were irradiated by 188 Re with single doses of 2.6 Gy-25.8 Gy. The effects of ?-particles on SMCs, such as effective irradiate doses, the period of inhibition for SMCs proliferation, the changes of cell proliferation rate and DNA synthesis rate, cell cycle progression and related gene expression, were investigated by cell count,-TdR incorporation, cell cycle progression analysis, cell viability and immunocytochemistry, respectivecy.

RESULTS:

?-particles irradiation with dose of 5.2 Gy could inhibit significantly SMCs proliferation. At dose of 20.6 Gy DNA synthesis inhibitory rate was 92%, SMCs proliferation rate was only 3%. Renoval of 188 Re did not abolish the inhibitory effects of ?-particles on SMCs proliferation. The expression of P53 was up regulation and PCNA was down regulation after irradiation.

CONCLUSION:

?-particles from 188 Re was significantly effective and permanent in inhibiting SMCs proliferation, and inhibitory effect was in dose-dependet manner ED50 was 5 Gy, the best dose to inhibit SMCs proliferation was 20 Gy. ?-particles irradiation induced SMCs to occur G 0/G 1 arrest, damaged the ability of SMCs reproliferation and led to cell clonogenic death. P53 and PCNA had regulatiory effects on SMCs proliferation after ?-particles irradiation.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2000 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2000 Type: Article