Research into the mechanism by which ATE curtails testosterone propionate-induced benign prostatic hyperplasia (BPH) in rats has revealed that A.tataricus exhibits therapeutic potential in BPH by enhancing apoptosis and suppressing inflammatory responses, as evidenced by substantial reductions in prostate weight, serum testosterone, and dihydrotestosterone levels, alongside inhibiting prostate epithelial thickening and the upregulation of proliferating cell nuclear antigen in rats. Here, PCNA is linked to benign prostatic hyperplasia.