Effects of estradiol on radiation-induced apoptosis of bone marrow hematopoietic cells in mice
10.3724/SP.J.1008.2008.00648
- Author:
Bai-Long LI
1
Author Information
1. Department of Radiation Medicine
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Bcl-2;
Extradiol;
Fas;
Hematopoietic cell;
Radiation injuries
- From:
Academic Journal of Second Military Medical University
2010;29(6):648-650
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of estradiol on 60Co γ-ray induced apoptosis of bone marrow hematopoietic cells of mice, and to discuss the related anti-irradiation mechanism. Methods: KM mice were randomly divided into 3 groups (15 mice/each group): control group (without radiation), pure radiation group and estradiol + radiation group (ER group). The pure radiation group was irradiated by 4.0 Gy γ-ray at a dose rate of 1.15Gy/min; the ER group was administered with 0.1 mg estradiol (IM) at 10 days before 4.0 Gy γ-ray radiation; and the control group received no special treatment. The apoptotic DNA segments of bone marrow hematopoietic cells were analyzed by DNA agarose gel electrophoresis; flow cytometry was used to examine the apoptosis rate of cells and expression of Fas and Bcl-2 at 4 h, 8 h, and 12 h after irradiation. Results: Eight hours after radiation, the apoptotic DNA segments were obviously increased and apoptotic DNA ladder appeared, which was not seen in the other 2 groups. The apoptosis rate of bone marrow hematopoietic cells in ER group was significantly lower than that in the pure radiation group at 4, 8, and 12 h after irradiation(P<0.01). Fas expression was only slightly elevated in the ER group than in the control group, but was markedly lower than that in pure radiation group(P<0.01), and showed no typical crest-time; Bcl-2 expression was significantly higher in the ER group than in the pure radiation group(P<0.01). Conclusion: Estradiol can decrease the apoptosis of mice bone marrow hematopoietic cells induced by γ-ray, probably through down-regulation of Fas and up-regulation of Bcl-2 expression.
