Background Brazilian berry is a fruit popularly known as "Jaboticaba," rich in bioactive compounds with antioxidant and anti-inflammatory properties. Senescence and overweight are increasing worldwide and are considered risk factors to prostatic pathogenesis mainly due to oxidative and inflammatory processes induction. Thus, this study aimed to evaluate the effect of two increasing doses of the patented jaboticaba peel extract (PJE) on oxidative-stress and inflammation in the prostate of aging or high-fat-fed aging mice. Methods PJE and/or high-fat diet (HFD) treatments started with 11-month-old mice and lasted 60 days. The levels or the immunoexpression of different inflammatory (nuclear factor κB [NFκB], CD3+, cyclooxygenase 2 [COX-2], toll-like receptor 4 [TLR4], phosphorylated signal transducers and activators of transcription 3 [pSTAT-3], tumor necrosis factor α [TNF-α], interleukin 6 [IL-6], and IL-1β) and oxidative-stress (catalase, superoxide dismutase 2 [SOD2], glutathione reductase [GSR], reduced glutathione, and glutathione peroxidase 3 [GPx3]) related molecules were analyzed by western-blotting, immunohistochemistry, and enzyme-linked immunosorbent assays. Results Both PJE doses reduced the levels of oxidative-stress-related molecules (GPx3, GSR, catalase), lipid peroxidation (4-hydroxynonenal), inflammatory mediators (COX-2, TNF-α, and pSTAT-3) and CD3+ T cells number, which were associated with the maintenance of the glandular morphological integrity in aging and HFD-fed-aging mice. Nevertheless, only the high PJE dose reduced the NFκB and TLR4 levels in aging mice; and SOD2, IL-6, and IL-1β levels in HFD-aging mice. Aging itself promoted an oxidative inflammation in the prostate, interfering in the levels of the different oxidative-stress, lipid peroxidation, and inflammatory mediators evaluated, in association with high incidence of prostate epithelial and stromal damages. The HFD intake intensified aging alterations, showing an unfavorable prostatic microenvironment prone to oxidative and inflammatory damages. Conclusions PJE exerted a dose-dependent effect controlling inflammation and oxidative-stress in aging and HFD-fed aging mice prostate. This fact contributed to prostate microenvironment balance recovery, preserving the tissue architecture of this gland. Thus, the PJE emerges as a potential therapy to prevent inflammation and oxidative stress in the prostate.

Brazilian berry extract (Myrciaria jaboticaba): A promising therapy to minimize prostatic inflammation and oxidative stress

Cyclooxygenase-2 (COX-2) has been implicated in prostate carcinogenesis, and recently it has been confirmed to be a molecular target of saturated fatty acids (SFAs). In the present study, we investigated the effect of stearic acid (SA) and palmitic acid (PA), two of the most abundant SFAs contained in dietary fat, on COX-2 expression in prostate epithelial cells and the signaling transduction pathway involved. First, we demonstrated that both SA and PA increased the mRNA and protein expression of COX-2, and consistently induced the activation of NF-κB in RWPE-1, BPH-1 and PC-3 prostate epithelial cell lines. The effect of SA and PA on COX-2 over-expression and NF-κB activation was in a dose-dependent manner, and PA was more potent than SA at the same concentration. Then, we demonstrated inhibition of NF-κB using its specific inhibitor strikingly attenuated PA-induced COX-2 expression. Toll-like receptor 4 (TLR4) was revealed to be expressed on RWPE-1, BPH-1 and PC-3 cell lines by PCR and immunofluorescence staining, and blocking its signaling significantly inhibited PA induced COX-2 over-expression and NF-κB activation. Taken together, we demonstrated that SFAs can up-regulate COX-2 expression in prostate epithelial cells, and this effect was mediated mainly through the TLR4/NF-κB signaling pathway.

Saturated fatty acids up-regulate COX-2 expression in prostate epithelial cells via toll-like receptor 4/NF-κB signaling.

Objective To investigate the effect and molecular mechanism of cyclooxygenase-2 (COX-2) on the benign prostatic hyperplasia (BPH) in rat model Methods Thirty-six SD rats were randomly divided into 3 groups:normal control (group A,n=12),BPH model (group B,n=12) and BPH+selective COX-2 inhibitor celecoxib (group C,n=12) At the 5th week after treatment, the weight of the prostates was measured, and the morphological changes were examined under light microscopeDetection of ki-67 and TUNEL in prostatic epithelial and stromal cells was undertaken to assess the proliferation and apoptosis statusThe protein and mRNA expression of COX-2,epidermal growth factor (EGF),basic fibroblast growth factor (bFGF) and transforming growth factor-β1 (TGF-β1) were analyzed by means of immunohistochemisty and RT-PCR Results The prostate index [prostate wet weight (mg)/rat body weight (g)] of group B was significantly higher compared with those in groups A and C (188±017 vs 170±009 and 174±016,P005)Remarkable prostatic hyperplasia in group B and epithelial cell atrophy in group C was noted by microscopyEpithelial and stromal cell proliferation indices (PI) of 3 groups were 0018± 0007 and 0007±0002, 0025±0006 and 0010±0004, 0017± 0006 and 0006± 0003,respectively;the PI of group B was significantly higher than those of groups A and C (P005)Apoptosis index (AI) of group C (0019±0005) was significantly higher than those of groups A and B (0015±0004 and 0013±0003,P005) The levels of COX-2 and EGF mRNA and protein in group B were up-regulated, while TGF-β1 was down-regulated compared with those of groups A and C (P005)There was no significant difference of bFGF expression among 3 groups (P005) Conclusions The increased expression of COX-2 may play an important role in the pathogenesis of BPH by modulating the expression of growth factors and affecting the proliferation and apoptosis of prostate cells

Study of effect and mechanism of cyclooxygenase-2 on the prostatic hyperplasia in rats

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Study of effect and mechanism of cyclooxygenase-2 on the prostatic hyperplasia in rats