Flaxseed Suppressed Prostatic Epithelial Proliferation in a Rat Model of Benign Prostatic Hyperplasia

Key Findings:

The androgens testosterone (T) and dihydrotestosterone (DHT) contribute to development of benign prostatic hyperplasia (BPH). Serum androgen T is converted by 5α-reductase to DHT. In rats treated with testosterone propionate (TP), flaxseed produced an anti-prostate enlargement effect. The effect was not mediated by a reduction of serum T levels. Flaxseed supplementation for 4 wk produced a trend toward reduced prostate weights and decreased ventral prostatic epithelial cell proliferation and epithelial height. These parameters were all increased by TP in the rat BPH model. An inhibition of 5α-reductase and the potent angiogenesis factor VEGF may be the mechanism of the effect of flaxseed on androgen homeostasis and androgen receptor expression.

ABSTRACT:

Benign prostatic hyperplasia (BPH), a disease occurring frequently among elderly males, is a slow progressive enlargement of the fibro muscular and epithelial structures of the prostate gland. Dietary factors may influence the prostate and exert an influence on prostatic growth and disease. The current study was undertaken to investigate the protective effect of dietary flaxseed supplementation against testosterone-induced prostatic hyperplasia in male rats.  Forty male Wistar rats were divided into 5 groups: (1) untreated control; (2) treatment with testosterone propionate (TP) to induce prostate enlargement; (3) TP-treated group fed a diet containing 5% milled flaxseed; (4) TP-treated group fed a diet containing 10% milled flaxseed; and (5) TP-treated group fed a diet containing 20 ppm finasteride. Treatment with TP significantly increased the absolute and relative weights of different prostatic lobes, serum testosterone (T), and testosterone/estradiol ratio, as well as prostatic vascular endothelial growth factor (VEGF) expression, RNA synthesis per cell, and epithelial cell proliferation, detected as Ki67 labeling. Histopathological examination did not reveal marked differences in acinar morphology in ventral prostate, whereas morphometric analysis showed significantly increased epithelial cell height. Co-administration of flaxseed or finasteride with TP significantly reduced prostatic VEFG, epithelial cell proliferation, and RNA/DNA ratio, along with a significant increase in serum T and testosterone/estradiol ratio compared with TP-only-treated rats. Our results indicate that flaxseed, similar to the 5α-reductase inhibitor finasteride, blocked TP-induced prostate enlargement in a rat model of BPH, likely through suppression of prostatic VEFG and cellular proliferation. (Authors abstract)