ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Asiatic acid mitigates testosterone-induced benign prostatic hyperplasia in rats via activation of PPAR-γ.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Investigation of the Protective Effect ofInternational journal of molecular sciences · 2026Article
- Green chemistry for prostate health: exploring nature's toolbox against cancer, inflammation, and hyperplasia.Molecular diversity · 2026Review
- Uroprotective effect of diarylpropionitrile versus finasteride on rat model of testosterone-induced prostatic hyperplasia.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
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3 authors.
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Abstract
Prostate enlargement due to benign prostate hyperplasia (BPH) is a common, progressive disorder in elderly males with increasing prevalence. It causes devastating lower urinary tract symptoms with no satisfactory medication. Asiatic acid (AA), a natural pentacyclic triterpenoid, is known to have antiproliferative, antioxidant, and anti-inflammatory activities. The aim of this study was to evaluate the possible preventive activities of AA against BPH induced by testosterone in rats. Finasteride (0.5 mg/kg) was used as a reference drug. AA (10 or 20 mg/kg) administration inhibited the rise in prostatic weight and index induced by testosterone. Histopathological staining proved that AA mitigated the pathological features of BPH induced by testosterone, which was reflected as lower glandular epithelial in AA-treated groups. Also, the administration of AA along with testosterone restored the redox valance by inhibiting lipid peroxidation, and MDA production, and restoring the activities of superoxide dismutase (SOD) and catalase (CAT) activities. Also, AA reduced prostate interleukin-6 (IL-6), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-α), and nuclear factor-kappa B (NF-κB) protein expression. In addition, AA modulated mRNA expression of Bax and Bcl-2 in favor of apoptosis. The effects of AA (20 mg/kg) were comparable to those of finasteride. Further, AA ameliorated the rise in insulin-like growth factor 1 receptor (IGF-1R) mRNA expression. This was associated with the enhancement of the prostatic content of PPAR-γ. It can be concluded that AA mitigated the features of BPH induced by testosterone in rats. This involves antioxidant, anti-inflammatory and pro-apototic activities of AA as well as its ability to down-regulate IGF-1R expression and enhance PPAR-γ concentration in prostatic tissues.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.