Roles of autophagy in androgen-induced benign prostatic hyperplasia in castrated rats

The present study investigated the role of androgen in the process of androgen-induced prostate hyperplasia in castrated rats and assessed the role of the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) pathway in this process. Furthermore, the extent to which autophagy may affect the level of androgen-induced benign prostatic hyperplasia was also explored. A total of 40 Sprague Dawley rats were randomly divided into four groups: Testosterone group, rapamycin group, 3-methyladenine (3-MA) group, and control group. The extent of hyperplasia in prostate tissue the apoptosis and autophagy were assayed. The prostate wet weight, volume and index in the testosterone group were significantly higher compared with the control group (P<0.05) and these factors were significantly lower in the rapamycin group compared with the testosterone group (P<0.05). HE staining demonstrated that prostate hyperplasia was obvious in the testosterone group. Western blotting revealed that caspase-3 levels were higher in the 3-MA group compared with the control group and Bcl-2 was higher in the testosterone group compared with the control group (P<0.05). Furthermore, in the rapamycin group, Bcl-2 protein expression levels were significantly lower than those in the testosterone group (P<0.05). The prostate tissue was analyzed using electron microscopy and autophagy bodies were identified in the rapamycin group. In the process of androgen-induced prostatic hyperplasia in castrated rats, the role of androgen may be related to the PI3K/Akt/mTOR signaling pathway. Rapamycin was able to inhibit the effect of testosterone and promoted prostate tissue hyperplasia by inhibiting the PI3K/Akt pathway. In addition to inhibiting apoptosis in prostate cells, androgen was able to induce rat prostate hyperplasia and may also be related to the promotion of the proliferation of prostate cells.