Rationale for the Use of Serenoa Repens Extract for Inflammatory Processes in the Prostate


Yurii Gurzhenko
Volodymyr Spyrydonenko


Phytotherapy remains one of the most popular methods of treating the initial stages of benign prostatic hyperplasia (BPH). One of the main mechanisms of action of herbal remedies is antiproliferative and anti-inflammatory effects of biologically active substances, which occur in the form of reducing the percentage of inflammatory infiltrates in intraoperative samples of prostate tissue.

The main direction of treatment of the initial stages of BPH is the appointment of plant inhibitors of 5α-reductase, the most famous of which is the extract of Serenoa repens (SESr). This plant extract has become widespread in the world and has one of the most reliable evidence bases based on many years of research.

In modern meta-analyzes of SESr, the mechanisms of action and evidence of its high clinical efficacy are quite clear. Scientific studies have shown that Serenoa repens can have selective antiandrogenic, anti-inflammatory, anti-edematous, prolactin-modulating and antiproliferative effects, the implementation of which in total can affect both the reduction of nodular hyperproliferation and prostate volume.

The mechanisms of realization of the effects of Serenoa repens extract in people with BPH are multifactorial, and some of them are not defined at all. In addition to the recognized antiphlogenic effects of inhibition of cyclooxygenase-2 and 5-lipoxygenases, modern studies have established the phenomenon of exposure at the level of apoptosis regulators in prostate cells.

The histological aspect of the combination of foci of benign hyperplasia with foci of chronic inflammation in prostate tissues is a factor of mutual burden, which causes rapid progression of BPH stages and the risk of prostate cancer (PC). The role of inflammation in the development of PC may be due to the presence of long-term elevated local levels of its mediators, which contribute to the formation of both genetic and metabolic conditions of acute apoptosis regulation. This is consistent with the assumption that changes in genes involved in inflammatory cascades can promote carcinogenesis, so the strategy of attempts to correct genetic polymorphism under BPH should contain a strong antiphlogenic component.

The pharmacological effects of Serenoa repens fully correspond to the pathogenetic essence of the prevention of the main prostate diseases of inflammatory and hyperplastic origin, as they are aimed at reducing the severity of two key processes: hyperproliferation and chronic inflammatory response, which successfully demonstrates the clinical use of Serenoa repens extract in long-term hypertensive therapy.


How to Cite
Gurzhenko, Y., & Spyrydonenko, V. (2022). Rationale for the Use of Serenoa Repens Extract for Inflammatory Processes in the Prostate. Health of Man, (1-2), 10–15. https://doi.org/10.30841/2307-5090.1-2.2022.263896
Topical issues
Author Biographies

Yurii Gurzhenko, Acad. O. F. Vozianov Institute of Urology NAMS of Ukraine

Yurii M. Gurzhenko,

Department of Sexopathology and Andrology

Volodymyr Spyrydonenko, Acad. O. F. Vozianov Institute of Urology NAMS of Ukraine

Volodymyr V. Spyrydonenko,

Department of Sexopathology and Andrology


Bostanci Y, Kazzazi A, Momtahen S, Laze J, Djavan B. Benign prostatic hyperplasia: Correlation between benign prostatic hyperplasia and inflammation. Curr Opin Urol. 2013;23(1):5–10. doi: 10.1097/MOU.0b013e32835abd4a.

Di Silverio F, Gentile V, De Matteis A, Mariotti G, Giuseppe V, Luigi PA, et al. Distribution of inflammation, premalignant lesions, incidental carcinoma in histologically confirmed benign prostatic hyperplasia: a retrospective analysis. Eur Urol. 2003;43(2):164-75. doi: 10.1016/s0302-2838(02)00548-1.

Kohnen PW, Drach GW. Patterns of inflammation in prostatic hyperplasia: a histologic and bacteriologic study. J Urol. 1979;121(6):755–60. doi: 10.1016/s0022-5347(17)56980-3.

Kramer G, Marberger M. Could inflammation be a key component in the progression of benign prostatic hyperplasia? Curr Opin Urol. 2006;16(1):25–9.

Lee KL, Peehl DM. Molecular and cellular pathogenesis of benign prostatic hyperplasia. J Urol. 2004;172(5 Pt 1):1784–91. doi: 10.1097/01.ju.0000133655.71782.14.

Untergasser G, Madersbacher S, Berger P. Benign prostatic hyperplasia: age-related tissue-remodeling. Exp Gerontol. 2005;40(3):121–8. doi: 10.1016/j.exger.2004.12.008.

Djavan B, Eckersberger E, Espinosa G, Kramerb G, Handisuryab A, Lee C, et al. Complex mechanisms in prostatic inflammatory response. Eur Urol Suppl. 2009;8:872–8. doi: 10.1016/j.eursup.2009.11.003.

Kramer G, Mitteregger D, Marberger M. Is benign prostatic hyperplasia (BPH) an immune inflammatory disease? Eur Urol. 2007;51(5):1202–16. doi: 10.1016/j.eururo.2006.12.011.

Steiner GE, Djavan B, Kramer G, Handisurya A, Newman M, Lee C, et al. The picture of the prostatic lymphokine network is becoming increasingly complex. Rev Urol. 2002;4(4):171–7.

Fibbi B, Penna G, Morelli A, Adorini L, Maggi M. Chronic inflammation in the pathogenesis of benign prostatic hyperplasia. Int J Androl. 2010;33:475–88. doi: 10.1111/j.1365-2605.2009.00972.x.

Crawford ED, Wilson SS, McConnell JD, Slawin KM, Lieber MC, Smith JA, et al. Baseline factors as predictors of clinical progression of benign prostatic hyperplasia in men treated with placebo. J Urol. 2006;175:1422–6. doi: 10.1016/S0022-5347(05)00708-1.

Mishra VC, Allen DJ, Nicolaou C, Sharif H, Hudd C, Karim OM, et al. Does intraprostatic inflammation have a role in the pathogenesis and progression of benign prostatic hyperplasia? BJU Int. 2007;100:327–31. doi: 10.1111/j.1464-410X.2007.06910.x.

Kang TW, Oh BR, Kim KW, Min KD, Kwon DD, Ryu SB. Clinical significance of prostatitis in patients with benign prostatic hyperplasia. Korean J Urol. 2003;44:278–82. doi: 10.4111/kju.2009.50.10.1014.

Kefi A, Koseoglu H, Celebi I, Yorukoglu K, Esen A. Relation between acute urinary retention, chronic prostatic inflammation and accompanying elevated prostate-specific antigen. Scand J Urol Nephrol. 2006;40(2):155–60. doi: 10.1080/00365590500497960.

Roehrborn CG, Kaplan SA, Noble WD, Lucia MS, Slawin KM, McVary KT, et al. The impact of acute or chronic inflammation in baseline biopsy on the risk of clinical progression of BPH: results from the MTOPS study. J Urol. 2005;173(Suppl): 346.

Baltaci S, Orhan D, Cogus C, Turkolmez K, Türkölmez K, Tulunay O, Gögüs O. Inducible nitric oxide synthase expression in BPH, low and high grade PIN and prostate carcinoma. BJU Int. 2001;88(1):100–03. doi: 10.1046/j.1464-410x.2001.02231.x.

Berger AP, Kurt K, Bektic J, Rogatsch H, Steiner H, Bartsch G, et al. Increased growth factor production in a human prostatic stromal cell culture model caused by hypoxia. Prostate. 2003;57(1):57–65. doi: 10.1002/pros.10279.

Gregoire R, Descazeaud A, Nicolayew N, Terry S, Sirab N, Vacherot F, et al. Inflammation in benign prostatic hyperplasia: a 282 patients’ immunohistochemical analysis. Prostate. 2009;69(16):1774–80. doi: 10.1002/pros.21027.

Kramer G, Steiner GE, Handisurya A, Stix U, Haitel A, Knerer B, et al. Increased expression of lymphocyte-derived cytokines in benign hyperplastic prostate tissue, identification of the producing cell types, and effect of differentially expressed cytokines on stromal cell proliferation. Prostate. 2002;52(1):43–58. doi: 10.1002/pros.10084.

Wang L, Liu Z, Yang L, Zhao H, Yue C, Li J, Han L. Expression of IL-6 and TNF-α in benign prostatic hyperplasia combined with histological inflammation. Discussion of Clinical Cases. 2016;3(1):11–5. doi: 10.5430/dcc.v3n1p11.

Gradini R, Realacci M, Petrangeli E, Di Silverio F, Russo M. Nitric oxide synthases in normal and benign hyperplastic human prostate: immunohistochemistry and molecular biology. J Pathol. 1999;189(2):224–9. doi: 10.1002/(SICI)1096-9896(199910)189:2<224::AID-PATH422>3.0.CO;2-K.

Bao B, Thakur A, Li Y, et al. The immunological contribution of NF-κB within the tumor microenvironment: A potential protective role of zinc as an anti-tumor agent. Biochim Biophys Acta. 2012;1825(2). doi:10.1016/j.bbcan.2011.11.002.

Tang J, Yang JC. Etiopathogenesis of benign prostatic hyperplasia. Indian J Urol. 2009;25(3):312–7. doi: 10.4103/0970-1591.56179.

Wen S, Chang H-C, Tian J, Shang Z, Niu Y, Chang C. Stromal Androgen Receptor Roles in the Development of Normal Prostate, Benign Prostate Hyperplasia, and Prostate Cancer. Am J Pathol. 2015;185(2):293–301.

Descazeaud A, Weinbreck N, Gregoire R, Vacherot F, Abbou CC, Labrousse F, et al. Transforming growth factor β-receptor II protein expression in benign prostatic hyperplasia is associated with prostate volume and inflammation. BJU Int. 2011;108(2 Pt 2):23–8. doi: 10.1111/j.1464-410X.2010.09699.x.

Dennis L, Lynch CF, Tornes JC. Epidemiologic association between prostatitis and prostate cancer. Urol. 2002;60(1):78–83. doi: 10.1016/s0090-4295(02)01637-0.

Di Silverio F, Bosman C, Salvatori M, Albanesi L, Pannunzi LP, Ciccariello M, et al. Combination therapy with rofecoxib and finasteride in the treatment of men with lower urinary tract symptoms (LUTS) and benign prostatic hyperplasia (BPH). Eur Urol. 2005;47:72–9. doi: 10.1016/j.eururo.2004.08.024.

Djavan B. Lower urinary tract symptoms benign prostatic hyperplasia: fast control of the patient’s quality of life. Urol. 2003;62(3 Suppl 1):6–14. doi: 10.1016/s0090-4295(03)00589-2.

Elkahwaji JE, Zhong W, Bushman W. Chronic bacterial infection and inflammation incite reactive hyperplasia in a mouse model of chronic prostatitis. Prostate. 2007;67(1):14–21. doi: 10.1002/pros.20445.

Klotz L, Vesprini D, Sethukavalan P, Jethava V, Zhang L, Jain S, et al. Long-term follow-up of a large active surveillance cohort of patients with prostate cancer. J Clin Oncol. 2015;33:272–7. doi: 10.1200/JCO.2014.55.1192.

Lowe F, Fagelman E. Phytotherapy in the treatment of benign prostatic hyperplasia. Curr Opin Urol. 2002;12:15. doi: 10.1007/s11934-002-0050-3.

Naber K, Weidner W. Chronic prostatitis: an infectious disease? J Antimicrob Chemother. 2000;46:157–61.

Nelson WG, De Marzo AM, Isaacs WB. Prostate cancer. N Engl J Med. 2003;349:366–81.

Dehong C, Ruonan S, Lei P, Jinze L, Yin H, Zeyu C, et al. Immune Cell Proinflammatory Microenvironment and Androgen-Related Metabolic Regulation During Benign Prostatic Hyperplasia in Aging. Front Immunol. 2022;13:842008. doi: 10.3389/fimmu.2022.842008.

Ficarra V, Rossanese M, Zazzara M, Giannarini G, Abbinante M, Bartoletti R, et. al. The role of inflammation in lower urinary tract symptoms (LUTS) due to benign prostatic hyperplasia (BPH) and its potential impact on medical therapy. Curr Urol Rep. 2014;15(12):463. doi: 10.1007/s11934-014-0463-9.

Forray C, Bard JA, Wetzel JM, Chiu G, Shapiro E, Tang R, et al. The α1-adrenergic receptor that mediates smooth muscle contraction in human prostate has the pharmacological properties of the cloned human α1с subtype. Mol Pharmacol. 1994;45(4):703–08.

Berges RR, Pientka L, Hufner K, Senge T, Jonas U. Male lower urinary tract symptoms and related health care seeking in Germany. Eur. Urol. 2001;39:682. doi: 10.1159/000052527.

Gravas S, Samarinas M, Zacharouli K, Karatzas A, Tzortzis V, Koukoulis, et al. The effect of hexanic extract of Serenoa repens on prostatic inflammation: results from a randomized biopsy study. World J Urol. 2019;37(3):539–44. doi: 10.1007/s00345-018-2409-1.

Vela-Navarrete R, Escribano-Burgos M, Farre AL, Garcia-Cardoso J, Manzarbeitia F, Carrasco C. Serenoa repens treatment modifies bax/bcl-2 index expression and caspase-3 activity in prostatic tissue from patients with benign prostatic hyperplasia. J Urol. 2005;173(2):507–10. doi: 10.1097/01.ju.0000150533.94952.25.

Zhou T, Yang Y, Zhang H, Che Y, Wang W, Lv H, et al. Serenoa Repens Induces Growth Arrest, Apoptosis and Inactivation of STAT3 Signaling in Human Glioma Cells. Technol Cancer Res Treat. 2014;14(6):12–6. doi: 10.7785/tcrt.2012.500417.

Navarrete RV, Garcia Cardoso JV, Barat A, Manzarbeitia F, Farré AL. BPH and inflammation: pharmacological effects of Permixon on histological and molecular inflammatory markers. Results of a double blind pilot clinical assay. Eur Urol. 2003;44(5):549–55. doi: 10.1016/s0302-2838(03)00368-3.

Plosker GL, Brogden RN. Serenoa repens (permixon). A review of its pharmacology and therapeutic efficacy in benign prostatic hyperplasia. Drugs Aging. 1996;9(5):379–95. doi: 10.2165/00002512-199609050-00008.

Paubert-Braquet M, Mencia Huerta JM, Cousse H, Braquet P. Effect of the lipidic lipidosterolic extract of Serenoa repens (Permixon) on the ionophore A23187-stimulated production of leukotriene B4 (LTB4) from human polymorphonuclear neutrophils. Prostaglandins Leukot Essent Fatty Acids. 1997;57(3):299–304. doi: 10.1016/s0952-3278(97)90548-2.

De Marzo AM. Pathological and molecular mechanisms of prostate cancerogenesis: implications for diagnosis, prevention and treatment. J Cell Biochem. 2004;91(3):459–77. doi: 10.1002/jcb.10747.

Latil A, Petrissans M-T, Rouquet J, Robert G, De la Taille A. Effects of hexanic extract of Serenoa repens (Permixon® 160 mg) on inflammation biomarkers in the treatment of lower urinary tract symptoms related to benign prostatic hyperplasia. Prostate. 2015;75(16):1857–67. doi: 10.1002/pros.23059.

Goldstraw MA, Fitzpatrick JM, Kirby RS. What is the role of inflammation in the pathogenesis of prostate cancer. BJU Int. 2007;172(5 Pt 2) 1–2. doi: 10.1097/01.ju.0000142058.99614.ff.

Palapattu GS, Sutcliffe S, Bastain PJ, Platz EA. Prostate carcinogenesis and inflammation: emerging insights. Carcinogenesis. 2004;26(7):1170–81. doi: 10.1093/carcin/bgh317.

Gorpinchenko II, Gurzhenko YUN, Klimenko PM, Shulyak AV, Spiridonenko VV. Issledovaniye Prospekt 2 (PROStamol: Perspektivy Kombinirovannoy Terapii) pri DGPZH. Zdorov’ye muzhchiny. 2012;(1):56–60.