Methyl jasmonate reduces testosterone-induced benign prostatic hyperplasia through regulation of inflammatory and apoptotic processes in rats
| Autor: | Olusoji J. Abiola, Solomon E. Owumi, Oluwatosin A. Adaramoye, Emiola Olubunmi Olapade-olaopa, Olubukola O Akanni, Oluyemi Akinloye |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Testosterone propionate Male medicine.medical_specialty Prostatic Hyperplasia Apoptosis Cyclopentanes Acetates urologic and male genital diseases Nitric Oxide Weight Gain Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Prostate Internal medicine medicine Animals Testosterone Oxylipins Rats Wistar Pharmacology Inflammation Methyl jasmonate biology urogenital system Chemistry Finasteride General Medicine Organ Size Hyperplasia medicine.disease Lipids Nitric oxide synthase 030104 developmental biology Endocrinology medicine.anatomical_structure 030220 oncology & carcinogenesis biology.protein Metabolic Detoxication Phase I Biomarkers |
| Zdroj: | Biomedicinepharmacotherapy = Biomedecinepharmacotherapie. 95 |
| ISSN: | 1950-6007 |
| Popis: | Background Phytotherapy is becoming a treatment option in management of diseases including benign prostatic hyperplasia (BPH). We have shown previously that methyl jasmonate (MeJA) ameliorated BPH, however the underlying mechanism of action remains unknown. This study was designed to investigate in mechanistic terms the protective role of MeJA in BPH. Methods BPH was induced by daily injections of testosterone propionate (TP) (3 mg/kg) for 28 days. Results The weight and organo-somatic weight of prostate in BPH rats were 6.8 and 5.1 times higher than castrated-control group, respectively. Inflammatory markers; prostatic myeloperoxidase and total nitric oxide were significantly increased in BPH group. The activity of aniline hydroxylase (Phase I drug metabolizing enzyme) was significantly increased in BPH rats by 22%. In BPH group, immuno-histochemistry revealed strong expression of prostatic inducible nitric oxide synthase, cyclooxygenase-2 and Bcl2, while mild expression of p53 and Bax were seen. Serum triglyceride and total cholesterol were significantly increased, while HDL-c was decreased in BPH. Interestingly, MeJA and finasteride (singly or combination) attenuated inflammatory indices and induced apoptotic parameters in BPH rats. Conclusion MeJA protects against TP-induced BPH via mechanisms that involve anti-inflammation, induction of apoptosis and inhibition of phase I drug metabolizing enzyme. |
| Databáze: | OpenAIRE |
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