Effects of long-term estrogen replacement treatment on the expression of bcl-2 and H-ras in rat endometrium.
- Author:
Xia XU
1
;
Mei-lian LIU
;
Jin LU
;
Ping XIE
;
Hui-ping SONG
Author Information
1. Department of Biochemistry, Biology Science and Techonology College, Central South University, Changsha 410078, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Endometrium;
metabolism;
Estradiol;
pharmacology;
Estrogen Replacement Therapy;
Female;
Genes, bcl-2;
Genes, ras;
Ovariectomy;
Proto-Oncogene Proteins c-bcl-2;
biosynthesis;
genetics;
RNA, Messenger;
biosynthesis;
genetics;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Time Factors;
ras Proteins;
biosynthesis;
genetics
- From:
Journal of Central South University(Medical Sciences)
2005;30(1):41-45
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effects of long-term estrogen replacement treatment (ERT) on the expression of bcl-2 and H-ras in rat endometrium.
METHODS:Thirty 5-month-old SD female rats were randomly divided into 3 groups: Control group ( sham operated and vehicle injected, n 10) , OVX group (OVX operated and vehicle injected, n = 10) , and ERT group (OVX operated and 17 beta-estradiol injected, n = 10). The rats were killed in the 13th week and the uteri were isolated and weighed, pathologically analyzed, and we measured the thickness of the endometrium. Immunochemistry and in situ hybridization analysis were used to examine the changes of bcl-2 and H-ras mRNA and Bcl and H-ras protein expression in the endometrium of the rats.
RESULTS:Uterine weight and endometrial thickness of OVX decreased much more than those of the control (P <0.01 ) and ERT rats (P < 0.01). One simple hyperplasia and one squamous metaplasia of endometrium were found in ERT rats. Quantitatively, bcl-2 and H-ras mRNA and Bcl and H-ras protein level of ERT were higher than those of OVX rats (P < 0.01 ), and there were no statistical significances between the ERT group and the control rats.
CONCLUSION:Long-term estrogen replacement can keep the endometrium from atrophy, and lead to the genesis of simple hyperplasia and squamous metaplasia of the endometriun, which can increase the risk of endometrial carcinomas. Estrogen may inhibit apoptosis and promote the proliferation of endometrial cells through increasing the expression of bcl-2 and H-ras mRNA and Bcl-H-ras proteins.
