Abstract
Benign prostatic hyperplasia (BPH) is one of the most common chronic diseases in men over the age of 50. Clinical studies have suggested that chronic inflammation is associated with BPH pathoprogression. Berberine (BB) is a natural compound found in Berberis vulgaris, Coptis chinensis and Phellodendron amurense. Although several studies have documented that BB may be effective for inflammation, the effects of the oral administration of BB on BPH are not fully understood. The effects of BB on chronic prostatic inflammation were evaluated in a testosterone-induced BPH animal model. Orally administered BB alleviated the pathological alterations induced by BPH and significantly suppressed the expression of inflammatory markers while enhancing the expression of antioxidant factors. Furthermore, BB regulated the activation of macrophages via NF-κB signaling pathway inhibition in the BPH rat model. The effects and underlying signaling pathway of BB in RWPE-1 cells exposed to macrophage conditioned medium (CM) were also demonstrated in vitro. While CM stimulation induced prostatic cell proliferation and upregulated the expression of inflammatory factors, BB exerted anti-proliferation and anti-inflammatory effects in RWPE-1 cells. These findings propose that BB suppresses androgen-dependent BPH development by targeting NF-κB-mediated pro-inflammatory signaling.
Highlights
Benign prostate hyperplasia (BPH) is common condition among men above the age of 50
As observed by hematoxylin and eosin (H&E) staining, rats from BPH group showed typical hyperplastic patterns, including multilayered epithelium and reduced glandular luminal area, and hyperplastic signs were descried in the Fina, BB 50, and BB 100 groups (Figure 1C)
TETP was significantly elevated in the BPH group, whereas a decrease was observed in the Fina, BB 50, and BB 100 groups (Figure 1D)
Summary
Benign prostate hyperplasia (BPH) is common condition among men above the age of 50. The cumulative incidence of BPH has been assumed to range from 50% in men aged 40–50 years up to 90% in men above the age of 80 [1]. It is recognized as mainly a proliferative disease, with prostate enlargement resulting in obstructive lower urinary tract symptoms and bladder outlet obstruction [2]. While prostatic hyperplasia seriously damages the quality of life, the pathogenesis of BPH remains unclear. It has commonly been assumed that androgen receptor (AR) signaling exerts a powerful effect upon the pathogenesis of BPH. AR signaling pathway is not the sole regulator of prostatic growth, as evidenced by the fact that over 25% of patients do not respond to 5ARIs [4]
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