Effect Of Bisphenol A On The Proliferation Of Human Uterine Leiomyoma Cells In Vitro

Objective:To investigate the expression of ERmRNA, IGFmRNA, VEGFmRNA and the suppressive effect of environmental estrogens bisphenol A on the proliferation of uterine leiomyoma cells in vitro. Our purpose was to investigate the effects of bisphenol A on the growth of human Uterine leiomyoma cell line in vitro and its provide of action.Methods:Uterine leiomyoma cells were cultured in vitro, after the action of letrozole with different concentration, MTT was used to examine the proliferative activity of uterine leiomyoma cells, which was mixed by different concentration bisphenol A. RT-PCR was used to determine the expression of the ERmRNA, IGFmRNA, VEGFmRNA.Results:1.Successful people cultivate human uterine leiomyoma cells in vitro and identified by immunocyto chemistry2.Blank control group uterine leiomyoma cells grow well. There was no significant difference between solvent control group and blank control group (P>0.05). Letrozole in a dose-time-dependent manner inhibited leiomyoma cell proliferation. The effect of 24h role was not obvious (P>0.05),48h increased at start steadily (P<0.05),72h at the most significant inhibitory effect (P<0.01), efficacy tended to saturation.25×10-7mol/L of letrozole had no effect on the expression of ERmRNA, IGFmRNA, VEGFmRNA, and estradiol synthesis and the proliferative activity in uterine leiomyoma cell (P>0.05). However,50×10-7mol/L,100×10-7mol/L of bisphenol A could inhibitor the expression of ERmRNA, IGFmRNA, VEGFmRNA,and to increase estradiol synthesis and the proliferation activity of uterine leiomyoma cells (P<0.05).Conclusion:1. Bisphenol A can increase proliferative activity of leiomyoma cells in vitroin a dose-time-dependent manner.2. Uterine leiomyoma cells in vitro can express ERmRNA, IGFmRNA, VEGFmRNA, and take advantage of growth factors may induced the emergence and growth of leiomyoma cells in vitro environment. 3. To be able to up-regulate ERmRNA, IGFmRNA, VEGFmRNA expression, promote apoptosis of bisphenol A cell in a dose-dependent manner.