Obstruction and neuropathic vesical dysfunction have the same effects on the urinary tract. These changes can best be understood by considering the effects of 1 a severe meatal stricture on the lower tract distal to the bladder neck , 2 a large obstructing prostate on the midtract bladder , and 3 an impacted stone in the ureter on the upper tract ureter and kidney. Hydrostatic pressure proximal to the obstruction causes dilation of the urethra.
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Thus, one could conclude that there are no alterations in the expression of steroid receptors that considerably affect benign hyperplastic tissue. However, since the more potent androgen DHT is generated in hyperplastic tissue, the use of anti-hormonal agents, which suppress functional activity of the AR, on the basis of pre-clinical findings will be further discussed. In this context, it is interesting to mention that the neuropeptide serotonin 5-HT down-regulates AR, thus preventing prostate branching [ 6 ].
The experiments with different 5-HT agonists yielded similar results regarding the androgen signalling pathway. It is a general opinion that neuroendocrine cells contribute to the progression of prostate cancer, whereas in BPH, they could have a different effect. Another compound which attenuates the effects of testosterone on BPH tissue is vanillic acid [ 7 ]. It was demonstrated that treatment with vanillic acid, which is also known as an anti-inflammatory agent, leads to reduction of prostate weight and induction of epithelial thickness. The authors have also performed in vitro experiments which largely confirmed the in vivo data.
However, it should be mentioned that investigations on the oncogenes Bcl-2 and Bcl-xl in BPH tissue after finasteride treatment have been carried out [ 8 ]. Interestingly, it has been proposed that the presence of the oncogene c-Jun in prostate fibroblasts is required for the in vitro growth of BPH-1 cells. Finasteride inhibitory effects on cellular proliferation were observed in the presence of c-Jun [ 9 ]. Concomitant use of dutasteride and testosterone led to growth inhibition of BPH-1 cells.
There are several options to interfere with androgen-induced growth of BPH cells when different nutrition ingredients or compounds that regulate cellular metabolism are used. For example, the widely used anti-diabetic agent metformin, which is known for its anti-proliferative and pro-apoptotic properties, was demonstrated to attenuate testosterone-induced BPH in rats [ 11 ].
Consequently, metformin acted as a pro-apoptotic factor through inhibition of the Akt pathway. IGFs regulate cell proliferation and apoptosis through a complex system which depends on the expression of receptors and binding proteins. Interestingly, higher levels of IGF binding protein-3 were measured in the stromal compartment of the prostate [ 13 ]. On the basis of these findings, it could be concluded that the IGF axis is a valid target for novel therapy approaches for BPH.
Hormonal regulation of BPH could be antagonized by chemopreventive agents. They are contained in fruits, broccoli, and green tea. Pomegranate fruit extract, which has anti-inflammatory and anti-oxidative properties, reduced testosterone increase in prostate weight and prevented hormonally induced histological changes [ 14 ]. Similarly, ginseng, which is used in traditional Korean herbal medicine, was evaluated as a potential drug in multiple diseases and was suggested for use in the experimental therapy of BPH [ 15 ].
Although the role of the environmental endocrine disruptor bisphenol needs to be investigated in more detail in appropriate BPH models, the evidence that it up-regulates aromatase should be taken into consideration with regard to BPH pathogenesis.