4.7 Article

Diacerein ameliorates testosterone-induced benign prostatic hyperplasia in rats: Effect on oxidative stress, inflammation and apoptosis

Journal

INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 100, Issue -, Pages -

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ELSEVIER
DOI: 10.1016/j.intimp.2021.108082

Keywords

Benign prostate hyperplasia; Apoptosis; Inflammation; Diacerein

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The study found that Diacerein (DIA) treatment significantly reduced prostate weight and index in testosterone-induced BPH rats, and improved prostatic biochemical and structural features. DIA treatment showed potential in limiting BPH progression through downregulation of inflammatory factors, proliferative markers, upregulation of apoptosis-related proteins, and enhancement of antioxidant mechanisms.
Benign prostatic hypertrophy (BPH) is a serious medical condition among elderly male population. BPH pathogenesis has been linked to inflammation, cellular proliferation, oxidative stress and apoptosis. Diacerein (DIA) is a FDA approved anthraquinone drug that is used to treat joint diseases such as osteoarthritis. DIA has been studied for its potent anti-inflammatory and antioxidant effects, yet its role in managing BPH has not been investigated. In this study, DIA administration for two weeks at 50 mg/kg in testosterone-induced BPH rats significantly reduced prostate weight and index. Moreover, prostatic biochemical and structural features in BPH rats were significantly improved upon DIA treatment. Mechanistically, DIA treatment associated prostatic antihyperplastic effects were linked to downregulation of Nrf-2/HO-1 axis, downregulation of inflammatory TNF-a, IL-1 beta, IL-6, downregulation of the cell proliferative marker PCNA and upregulation of caspase-3 levels. In addition, DIA treatment upregulated prostatic antioxidant GSH, the enzymatic SOD and CAT activities and reduced prostatic lipid peroxidation levels. Altogether, the present study provides evidence that DIA treatment might limit BPH progression via its potent anti-oxidant, anti-inflammatory, anti-proliferative and apoptosis inducing effects.

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