Serenoa Repens, Lycopene and Selenium: A Triple Therapeutic Approach to Manage Benign Prostatic Hyperplasia
L. Minutoli, A. Bitto, F. Squadrito, H. Marini, N. Irrera, G. Morgia, A. Passantino and D. Altavilla
Affiliation: Department of Clinical and Experimental Medicine, Torre Biologica 5th floor, c/o AOU Policlinico G. Martino, Via C. Valeria Gazzi, 98125, Messina, Italy.
Keywords: Apoptosis, BPH, cytokines
Benign prostatic hyperplasia (BPH) is a major health concern that is likely to have an increasing impact in line
with the gradual aging of the population. BPH is characterized by smooth muscle and epithelial proliferation primarily
within the prostatic transition zone that can cause a variety of problems for patients, the most frequent are the lower urinary
tract symptoms. BPH is thought to involve in disruption of dihydrotestosterone (DHT)-supported homeostasis between
cell proliferation and cell death, and, as a result, proliferative processes predominate and apoptotic processes are inhibited.
Phytotherapeutic supplements, mainly based on Saw Palmetto-derived Serenoa Repens (SeR), are numerous and
used frequently. Serenoa Repens reduces inflammation and decreases in vivo the androgenic support to prostatic cell
growth. Furthermore, SeR stimulates the apoptotic machinery; however, data supporting efficacy is limited, making
treatment recommendations difficult. Besides SeR, selenium (Se), an essential trace element mainly functioning through
selenoproteins and able to promote an optimal antioxidant/oxidant balance, and lycopene (Ly), a dietary carotenoid synthesized
by plants, fruits, and microorganisms with a strong antioxidant activity, has been shown to exert beneficial effects
in prostate disease. SeR is frequently associated with Ly and Se, in order to increase its therapeutic activity in benign
prostatic hyperplasia (BPH). It has been shown that the Ly-Se-SeR association has a greater and enhanced antiinflammatory
activity that might be of particular interest in the treatment of BPH. The Ly-Se-SeR association is also more
effective than SeR alone in reducing prostate weight and hyperplasia, in augmenting the pro-apoptotic Bax and caspase-9
and blunting the anti-apoptotic Bcl-2 mRNA. In addition, Ly-Se-SeR more efficiently suppresses the EGF and Vascular
Endothelial Growth Factor (VEGF) expressions in hyperplastic prostates. Therefore, SeR particularly when combined
with Se and Ly may have a greater potential for the management of benign prostate hyperplasia.
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