During the differentiation and development of the male urogenital system, sufficient testosterone and intact androgen receptors exert critical regulatory effects. Testosterone is converted into more potent dihydrotestosterone (DHT) under the action of 5α-reductase. The binding of DHT to androgen receptors modulates the expression of downstream genes, thereby governing the differentiation and development of the genital tubercle. Consequently, functional impairment of 5α-reductase disrupts the normal development of the male urogenital system. Finasteride, a widely used clinical agent for benign prostatic hyperplasia, interferes with androgen metabolism and normal cellular signal transduction. In animal model establishment, finasteride selectively inhibits 5α-reductase type 2, blocks the conversion of testosterone to DHT, and ultimately impairs the normal fusion of urethral folds in male fetal rats.

SD rats (male and female, 3 months old)
Modeling method: On the 8th day after conception, female rats were intragastrically administered with finasteride. The hypospadias model was successfully established one week later.
Evaluation index: HE staining

Urethral HE staining