Abstract
BPH is a disease prevalent among elderly men that is characterized by abnormal proliferation of prostatic epithelial and stromal tissues. No effective treatment exists for BPH owing to lack of a clear understanding of its molecular etiology. Although several studies have reported therapeutic effects of baicalin against numerous diseases, including prostate cancer, its beneficial effects on BPH have not yet been explored. The present study investigated the therapeutic effects of baicalin on the development of BPH and its mechanism of action. We established a testosterone-treated BPH animal model and DHT-stimulated prostate cell lines, including RWPE-1 and WPMY-1. Administration of baicalin ameliorated the pathological prostate enlargement, suppressed the production of DHT, and inhibited the activity of 5α- reductase Type II in the animal model. BC exerted these effects via its anti-proliferative effects by restoring the Bax/Bcl-2 ratio, activating caspase-3 and caspase-8, and inducing the phosphorylation of AMPK. In vitro studies using DHT-stimulated prostate cells demonstrated an up-regulation of BPH-related and proliferation markers, whereas baicalin clearly reduced the overexpression of AR, PSA, PCNA, and Bcl-2. These results suggested that baicalin could suppress androgen-dependent development of BPH both in vivo and in vitro by inducing apoptosis.
Highlights
Benign prostate hyperplasia (BPH) and prostate cancer (PCa) are age-related chronic diseases that initiate at an early age and progress slowly [1]
Numerous studies have used Testosterone propionate (TP)-treated rats as a model to study BPH owing to its characteristic resemblance to the actual disease [17, 18]
As compared to the control group, abnormal DHT levels were detected by ELISA in the BPH group
Summary
Benign prostate hyperplasia (BPH) and prostate cancer (PCa) are age-related chronic diseases that initiate at an early age and progress slowly [1]. Several clinical studies have suggested a link between BPH and PCa owing to a number of similarities between the two. It has been speculated that two diseases have similar clinical presentation and pathogenic mechanisms. Both are characterized by rapid proliferation of prostatic cells. Despite the existence of a lot of controversy between the two diseases, common pathophysiological risk factors include chronic inflammation, metabolic disturbances, and hormonal association [2, 3]. Epidemiological studies have suggested that since the incidence and prevalence of two diseases increase with age, their pathoprogression is hormone dependent and involved in chronic prostatic inflammation [4]
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