Effect of TanshinoneⅡA on Experimental Endometriosis in Rats
10.3870/j.issn.1004-0781.2016.06.014
- VernacularTitle:丹参酮ⅡA对子宫内膜异位症模型大鼠的治疗作用?
- Author:
Lili ZHENG
;
Wei LI
;
Dou HUANG
;
Lin LUO
;
Xiaohong LUO
;
Yuan LI
- Publication Type:Journal Article
- Keywords:
TanshinoneⅡA;
Endometriosis;
Cell apoptosis
- From:
Herald of Medicine
2016;35(6):612-615
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of TanshinoneⅡA( TanⅡA) on endometriosis( EMS) rat model and study the possible mechanism. Methods EMS rat model was established by autologous endometrium transplantation. EMS rats were randomly divided into five groups: high-, medium-, low-dose TanⅡA group, mifepristone group and model control group( n=10), the other ten normal rats as normal control group.The rats in the model control group and normal control group were given 0.9% sodium chloride solution. The rats in the mifepristone group were given 25 mg . kg-1 . d-1 mifepristone. The rats in the high-, medium-, low-dose TanⅡA groups were given 30, 20 and 10 mg.kg-1.d-1 TanⅡA, respectively.Four weeks after the treatment, the volume of endometriotic implants in each rat was measured. Pathological changes of ectopic endometrium were observed under light microscope.Expression levels of Bcl-2, Bax and Caspase-9 in ectopic endomembrane of rats were determined by Western blotting. Results High and medium dose TanⅡA and mifepristone significantly reduced the volume of ectopic lesions(P<0.05).As compared with model control group, the inhibition rate of the ectopic lesions in low-, medium-, high-dose TanⅡA groups and mifepristone group was 17.81%, 57.78%, 58.88% and 64.12%, respectively.High and medium dose TanⅡA and mifepristone promoted atrophy of ectopic endometrium, inhibited the expression of Bcl-2 protein and promoted the expression of Bax and Caspase-9 in ectopic tissues( P<0.05) . Conclusion TanⅡA significantly decreases the size of ectopic lesions in rats, possibly through reducing the expression of Bcl-2 and increasing the expression of Bax and Caspase-9 to regulate cell apoptosis.
