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Ellagic acid improves benign prostate hyperplasia by regulating androgen signaling and STAT3.
Park, Woo Yong; Song, Gahee; Park, Ja Yeon; Ahn, Kwang Seok; Kwak, Hyun Jeong; Park, Jinbong; Lee, Jun Hee; Um, Jae-Young.
Afiliación
  • Park WY; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul, Republic of Korea.
  • Song G; Department of Pharmacology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
  • Park JY; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul, Republic of Korea.
  • Ahn KS; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul, Republic of Korea.
  • Kwak HJ; Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul, Republic of Korea.
  • Park J; Department of Life Science, College of Natural Sciences, Kyonggi University, Suwon, Republic of Korea.
  • Lee JH; Department of Pharmacology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
  • Um JY; Department of Sasang Constitutional Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Cell Death Dis ; 13(6): 554, 2022 06 17.
Article en En | MEDLINE | ID: mdl-35715415
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_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.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Hiperplasia Prostática / Propionato de Testosterona Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: Cell Death Dis Año: 2022 Tipo del documento: Article Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Hiperplasia Prostática / Propionato de Testosterona Tipo de estudio: Prognostic_studies Límite: Animals / Humans / Male Idioma: En Revista: Cell Death Dis Año: 2022 Tipo del documento: Article Pais de publicación: Reino Unido