MP06-05 PUNICALAGIN MITIGATES TESTOTERONE PROPIONATE (TP)-INDUCED BENIGN PROSTATIC HYPERPLASIA (BPH) IN CASTRATED RATS VIA OXIDO-INFLAMMATORY AND APOPTOTIC MECHANISM

You have accessJournal of UrologyBenign Prostatic Hyperplasia: Basic Research & Pathophysiology (MP06)1 Apr 2020MP06-05 PUNICALAGIN MITIGATES TESTOTERONE PROPIONATE (TP)-INDUCED BENIGN PROSTATIC HYPERPLASIA (BPH) IN CASTRATED RATS VIA OXIDO-INFLAMMATORY AND APOPTOTIC MECHANISM Monsuru Sanni* and Oluwatosin Adaramoye Monsuru Sanni*Monsuru Sanni* More articles by this author and Oluwatosin AdaramoyeOluwatosin Adaramoye More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000000820.05AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Inflammation and oxidative stress plays a central role in the etiology and progression of Benign Prostatic Hyperplasia (BPH), a common urological disorder in aged men. Punicalagin (PN), a bioactive compound found in the pomegranate (Punica granatum), exhibits potent antioxidant and anti- inflammatory properties. Here, we are reporting the oxido-inflammatory and apoptotic effect of Punicalagin (PN) on testosterone propionate (TP)-induced benign prostatic hyperplasia (BPH) in castrated Wistar rats. METHODS: Castrated Wistar rats weighing (180–240 g) had exogenous, daily administration of testosterone propionate (TP) at 3 mg/kg for four weeks, and staggered doses of PN (50 mg/kg) and Finasteride (FT) at (10 mg/kg) three times weekly for four weeks. The rats were assigned into five groups of six animals each: castrated control, castrated rats that received TP [BPH], castrated rats that received TP and PN [BPH + PN], castrated rats that received TP and FT [BPH + FT], and castrated rats that received TP, PN and FT [BPH + PN + FT]. Prostatic tissues were collected for biochemical and immunohistochemical examination. Prostatic oxidative status (SOD, CAT, GSH, GST, GPx and MDA), Inflammations (NO and MPO) were assessed biochemically and immunohistochemically (COX2 and iNOS). Testosterone level was assessed using ELISA method. Prostatic cell death regulators (p53, Bcl-2 and Bax) and prostatic receptors (AR and ER) were determined using immunohistochemistry. RESULTS: Our data showed that PN significantly (p<0.05) reduced the prostatic weights and testosterone level in BPH rats. The decreased activities of SOD, CAT and GPx were significantly (p<0.05) increased by PN in BPH rats. The increased level of LPO and NO and activities of MPO and GST in BPH rats were significantly (p<0.05) reduced by PN indicating antioxidant and anti-inflammatory activities. PN also suppressed the expression of AR, ER, COX2 and iNOS which further suggest anti-inflammatory activities. PN suppressed the expressions of Bcl-2 and increased the expression of Bax and p53 suggesting anti-apoptotic effects. CONCLUSIONS: PN mitigates testosterone propionate induced BPH via mechanism involving oxido-inflammatory and apoptotic effects in castrated rats. Source of Funding: None © 2020 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 203Issue Supplement 4April 2020Page: e52-e53 Advertisement Copyright & Permissions© 2020 by American Urological Association Education and Research, Inc.MetricsAuthor Information Monsuru Sanni* More articles by this author Oluwatosin Adaramoye More articles by this author Expand All Advertisement PDF downloadLoading ...