ArticleMolecular biology reports2025
Curcumin targets miR-21-3p: promising therapeutic strategy for treatment of benign prostatic hyperplasia.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundIt is still unclear if curcumin's therapeutic effect in benign prostatic hyperplasia (BPH) is linked to microRNA regulation. This study explored the potential role of miR-21-3p in curcumin-induced anti-inflammatory and antiproliferative effects in BPH. METHODS AND
resultsTwenty-four male adult rats were grouped randomly into four groups: normal control group, BPH group, BPH group treated with curcumin and BPH group treated with finasteride as a reference drug. The BPH model was experimentally induced by s.c. injection of testosterone enanthate (3 mg/ Kg) five times a week for two weeks, curcumin and finasteride were given orally, parallel to testosterone injection. The results showed that curcumin-induced decrease in prostate index and prostate-specific antigen (PSA)-like protein expression were associated with downregulation of miR-21-3p compared with the BPH untreated group. Immunohistochemical staining revealed increased SIRT1 expression and decreased NF-κB and TNF-α expression in the curcumin-treated group compared to the BPH untreated group. In addition, β-catenin protein expression, measured by Western blotting, as well as β-catenin-linked signaling proteins, LRP6 and c-Myc, were suppressed in the curcumin group. The results obtained with curcumin treatment were comparable to those with finasteride treatment. Our data were supported by histopathological findings.
conclusionsThe current study demonstrated that curcumin alleviated the inflammatory manifestations of BPH by targeting the pro-inflammatory microRNA miR-21-3p, thereby upregulating SIRT1 and downregulating the pro-inflammatory mediators NF-κB and TNF-α. Furthermore, the anti-proliferative effect of curcumin may be attributed to the inhibition of the β-catenin signaling pathway.
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