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Updated: Jun 5, 2026
Murine Prostate Micro-dissection and Surgical Castration
Published on: May 11, 2016
Possible mechanism of benign prostatic hyperplasia induced by androgen-estrogen ratios in castrated rats
Liu Xiang-Yun1, Xu Ying-Wen, Xie Chen-Jing
1Department of Pharmacology and Toxicology, Shanghai Institute of Planned Parenthood Research, National Evaluation Centre for the Toxicology of Fertility Regulation Drugs, Shanghai 200032, China.
Objectives:
To explore the role of androgen-estrogen balance in benign prostatic hyperplasia (BPH) induced by varying doses of estradiol/testosterone propionate (E(2)/TP) in castrated rats.
Materials And Methods:
A total of 222 rats were divided into 37 groups at random, including 35 groups of different E(2)/TP, one control, and one castrated group. All 37 groups except the control group were castrated, for eliminating endogenesis of testosterone in rats. The treated groups were administered testosterone propionate (TP; at the dosages of 0.15, 0.74, 3.7, 18.5, and 92.6 mg/kg), combined with estradiol (E(2); at the dosage of 0, 0.4, 2, 10, 50, 250, and 1250 µg/kg) diluted in vegetable oil for 30 days, respectively, whereas the control groups received only vegetable oil. All prostate specimens were removed under anesthesia, then fixed and embedded in paraffin, for measuring the organ quotient, volume, area of prostate glandular cavity, and the height of prostate epithelia.
Results:
When the dosages of TP were 0.15, 3.7, 18.5, and 92.6 mg/kg, the degree of prostatic hyperplasia had no obvious dose-effect relationship with E(2). When TP was 0.74 mg/kg, with the increase of the dosage of E(2), the volume and quotient of prostate were increasing. However, when the dosage of E(2)exceeded 50 µg/kg, E(2)/TP was 5/74, the prostatic volume did not increase obviously.
Conclusion:
The proper levels of E2/TP play an important role in the pathogenesis of BPH. In rats, the balance point of E(2)/TP is 5/74.
