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조회655

동국대학교

Redox Biol., Available online 11 July 2023 | https://doi.org/10.1016/j.redox.2023.102816 Antioxidant mitoquinone suppresses benign prostatic hyperplasia by regulating the AR–NLRP3 pathway

Bo-Ram Jin a, Chae-Young Lim ^b, Hyo-Jung Kim^a, Minho Lee^b, Hyo-Jin An^a,c

^aDepartment of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul, 02447, Republic of Korea
^bDepartment of Life Science, Dongguk University-Seoul, 32 Dongguk-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do, 10326, Republic of Korea
^cDepartment of Integrated Drug Development and Natural Products, Graduate School, Kyung Hee University, Seoul, 02447, Republic of Korea

Corresponding authors: Minho Lee, Hyo-Jin An

Abstract

Mitoquinone (MitoQ), a mitochondria-targeted antioxidant, has been used to treat several diseases. The present study aimed to investigate the therapeutic effects of MitoQ in benign prostatic hyperplasia (BPH) models and their underlying molecular mechanisms. In this study, we determined that MitoQ inhibited dihydrotestosterone (DHT)-induced cell proliferation and mitochondrial ROS by inhibiting androgen receptor (AR) and NOD-like receptor family pyrin domain-containing 3 (NLRP3) signaling in prostate epithelial cells. Molecular modeling revealed that DHT may combine with AR and NLRP3, and that MitoQ inhibits both AR and NLRP3. AR and NLRP3 downregulation using siRNA showed the linkage among AR, NLRP3, and MitoQ. MitoQ administration alleviated pathological prostate enlargement and exerted anti-proliferative and antioxidant effects by suppressing the AR and NLRP3 signaling pathways in rats with BPH. Hence, our findings demonstrated that MitoQ is an inhibitor of NLPR3 and AR and a therapeutic agent for BPH treatment.

논문정보

형식Research article
게재일2023년 07월 (BRIC 등록일 2023-07-20)
연구진국내 연구진
분야 의약학 > 약학

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