摘要
目的探讨不同剂量睾酮干预小鼠心肌细胞衰老中p16INK4a的表达。方法用1μmol/L,100nmol/L,10 nmol/L3种剂量睾酮干预自然衰老的小鼠心肌细胞,检测各组衰老相关β-半乳糖甘酶染色阳性细胞率,细胞周期分布,p16INK4amRNA及蛋白表达。结果与衰老心肌细胞相比,1μmol/L,100 nmol/L,10 nmol/L睾酮可剂量依赖性的降低衰老相关β-半乳糖甘酶染色阳性细胞率及细胞G0/G1期比例(P<0.05)。睾酮干预亦可剂量依赖性地下调p16INK4amRNA及蛋白表达。结论1μmol/L,100 nmol/L,10 nmol/L睾酮可通过剂量依赖性地减少p16INK4a的表达,抑制小鼠心肌细胞衰老。
Objective To investigate the effects of testosterone on the murine aging cardiac myocytes and the possible mechanism. Methods Natural aging murine cardiac myocytes were treated with 1 μmol/L, 100 nmol/L and 10 nmol/ L of testosterone and the positive rate of senescence - associated β galactosidase staining, distributions of cell cycles, and the expressions of p16^INK4a were measured. Results Compared with the aging cardiac myocytes, 1 μmol/L, 100 nmol/L and 10 nmol/L testosterone reduced the proportions of SA β - gal - positive cells and diminishes G0/G1 phase of cell cycles in a dose -dependent way（P 〈0.05 ）. Testosterone administration also induced a dose -dependent down -regulation of the expressions of p16^INK4a mRNA and protein, which was blocked by fultamide （P 〈0.05）. Conclusion 1 μmol/L, 100 nmol/ L and 10 nmol/L testosterone attenuated the senescence of natural aging murine cardiac myocytes in a dose - dependent way, and this effect may be partly achieved by decreasing the expression of p16^INK4a via the AR pathway.
出处
《广东医学》
CAS
CSCD
北大核心
2009年第6期859-861,共3页
Guangdong Medical Journal
基金
国家973项目子课题(编号:2007CB507400)
