The prostate has a very close relationship with androgens. The growth and development of the prostate, the integrity of its structure and function, and the occurrence of pathological changes all depend on the action of androgens. Androgens acting on the prostate are converted into dihydrotestosterone under the catalysis of 5α-reductase, which is then aromatized into estradiol. Dihydrotestosterone is the most potent androgen in the human body, with an activity 2–3 times that of testosterone, and its binding capacity to androgen receptors is 4–5 times that of testosterone. Androgens bind to corresponding receptors on prostate cells, causing an imbalance between proliferation and apoptosis of prostate cells by inhibiting apoptosis and promoting cell proliferation, ultimately inducing prostatic hyperplasia. The testes are the main source of androgens for the prostate. Orchiectomy combined with low-dose exogenous androgen supplementation can disrupt the body\'s endogenous hormonal balance, thereby inducing prostatic hyperplasia.

SD rats (male, 6–8 weeks old)
Modeling method: 7 days after castration, testosterone propionate was injected subcutaneously continuously for 4 weeks, and the benign prostatic hyperplasia model was successfully established.
Evaluation indicators:

Prostatic index

HE staining of the prostate