Effect of Serenoa repens, Lyocopene, and Selenium on Proinflammatory IκB-α Phenotype Activation: An In Vitro And In Vivo Comparison Study

OBJECTIVES To investigate the antiinflammatory activity of Serenoa repens (SeR), LY, and) on proinflammatory phenotype in rat peritoneal macrophages (Ms) stimulated with Salmonella enteritidis lipopolysaccharid (LPS) and in the prostate of rats with partial bladder outlet obstruction. SeR, combined with other compounds, such as LY and Se is used to relieve symptoms associated with benign prostatic hyperplasia (BPH). Inflammation plays a pivotal role in the pathogenesis of BPH and represents a target for anti-BPH drugs. METHODS After stimulation with 1 mu g/mL of LPS, peritoneal rat M Phi s were coincubated with LY (2 mu g/mL), Se (0.03 mu g/mL), and SeR (10 mu g/mL), alone or in association (LY-Se-SeR) and with RPMI. Inducible cyclooxygenase (COX-2), 5-lypoxygenase (5-LOX), inducible nitric oxide synthase (iNOS), and inhibitor kappa B alpha (I kappa B-alpha) protein were evaluated by Western blot. Nuclear factor-kappa B (NF-kappa B) binding activity was measured by electrophoretic mobility shift assay. Tumor necrosis factor-alpha (TNF-alpha) gene expression was investigated by real-time polymerase chain reaction. We also evaluated malondialdehyde (MDA) and nitrite levels. RESULTS LPS stimulation produced a proinflammatory phenotype in rat peritoneal M Phi s. LY, Se, and SeR inhibited the inflammatory cascade, but the Ly-Se-SeR association caused a greater inhibitory effect on the expression of COX-2, 5-LOX, and iNOS. The Ly-Se-SeR association showed a higher efficacy in reducing the loss of I kappa B-alpha, the increased NF-kappa B binding activity, the enhanced mRNA levels of TNF-alpha, the elevated MDA, and nitrite content. The LY-Se-SeR association in vivo caused a greater inhibitory effect on prostate inflammation induced in rats by partial bladder outlet obstruction. CONCLUSIONS The LY-Se-SeR association might be useful in the treatment of BPH. UROLOGY 77: 248.e9 -248.e16, 2011. (C) 2011 Elsevier Inc.