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Ellagic acid improves benign prostate hyperplasia by regulating androgen signaling and STAT3.
- Source :
-
Cell death & disease [Cell Death Dis] 2022 Jun 17; Vol. 13 (6), pp. 554. Date of Electronic Publication: 2022 Jun 17. - Publication Year :
- 2022
-
Abstract
- Benign prostate hyperplasia (BPH) is an age-related disease in men characterized by the growth of prostate cells and hyperproliferation of prostate tissue. This condition is closely related to chronic inflammation. In this study, we highlight the therapeutic efficacy of ellagic acid (EA) for BPH by focusing on the AR signaling axis and STAT3. To investigate the effect of EA on BPH, we used EA, a phytochemical abundant in fruits and vegetables, to treat testosterone propionate (TP)-induced BPH rats and RWPE-1 human prostate epithelial cells. The EA treatment reduced prostate weight, prostate epithelial thickness, and serum DHT levels in the TP-induced BPH rat model. In addition, EA improved testicular injury by increasing antioxidant enzymes in testis of the BPH rats. EA reduced the protein levels of AR, 5AR2, and PSA. It also induced apoptosis by regulating Bax, Bcl&#95;xL, cytochrome c, caspase 9, and caspase 3 with increasing mitochondrial dynamics. Furthermore, EA reduced the expression of IL-6, TNF-α, and NF-κB, as well as phosphorylation of STAT3 and IκBα. These findings were also confirmed in TP-treated RWPE-1 cells. Overall, our data provide evidence of the role of EA in improving BPH through inhibition of AR and the STAT3 pathway.<br /> (© 2022. The Author(s).)
- Subjects :
- Androgens pharmacology
Animals
Ellagic Acid adverse effects
Humans
Hyperplasia pathology
Male
Plant Extracts pharmacology
Prostate metabolism
Rats
Rats, Sprague-Dawley
STAT3 Transcription Factor metabolism
Prostatic Hyperplasia chemically induced
Prostatic Hyperplasia drug therapy
Prostatic Hyperplasia metabolism
Testosterone Propionate adverse effects
Subjects
Details
- Language :
- English
- ISSN :
- 2041-4889
- Volume :
- 13
- Issue :
- 6
- Database :
- MEDLINE
- Journal :
- Cell death & disease
- Publication Type :
- Academic Journal
- Accession number :
- 35715415
- Full Text :
- https://doi.org/10.1038/s41419-022-04995-3