We found that QTC, especially when administered in high-dosages, had a significant inhibitory effect on bladder weight gain and overexpression of NGF, bFGF, and TGF-<i>β</i>1 in rats with BPH.
When culture supernatants of the proliferating prostate stromal cells were added to BPH epithelial cells, the latter multiplied, and expression of cyclin D1, FGF2 and Bcl-2 increased.
In this work, the bFGF receptors (FGFR1, FGFR2-IIIc and FGFR3) genes expression was evaluated to study the correlation between the expression of bFGF receptors and induction of BPH.
Therefore IL-8 produced by prostatic epithelial cells can induce FGF2, a potent stromal and epithelial growth factor, and in this manner promote the abnormal proliferation of the prostatic transition zone that is critical in the pathogenesis of BPH.
By immunohistochemistry done with a polyclonal antibody to recombinant FGF-2 on paraffin sections, FGF-2 was localized in fibroblasts, endothelial cells and smooth muscle cells of tissue samples of BPH.
Basic fibroblast growth factor (bFGF) and transforming growth factor beta 1 (TGFbeta1) are potential autocrine growth regulators of the prostatic stroma, and therefore may play a role in the development of benign prostatic hyperplasia (BPH).
With digoxigenin-labeled oligonucleotides in nonradioactive in situ hybridization, the presence of mRNA for bFGF was shown in smooth muscle cells of the stroma, suggesting that these cells are the main source of bFGF in BPH.
The level of bFGF has been reported to be elevated in benign prostatic hyperplasia (BPH), compared with normal prostate, suggesting that the growth factor may play a role in this disease of the prostate.