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Electric Stimulation Hyperthermia Relieves Inflammation via the Suppressor of Cytokine Signaling 3-Toll Like Receptor 4 Pathway in a Prostatitis Rat Model

The World Journal of Men′s Health 2020년 38권 3호 p.359 ~ 369
Zhu Guan Qun, 전승환, 이규원, Tian Wen Jie, 조혁진, 하유신, 홍성후, 이지열, 문명건, 문성희, 김세웅, 배웅진,
소속 상세정보
 ( Zhu Guan Qun ) - Catholic University College of Medicine Department of Urology
전승환 ( Jeon Seung-Hwan ) - Catholic University College of Medicine Department of Urology
이규원 ( Lee Kyu-Won ) - Catholic University College of Medicine Department of Urology
 ( Tian Wen Jie ) - Catholic University College of Medicine Department of Urology
조혁진 ( Cho Hyuk-Jin ) - Catholic University College of Medicine Department of Urology
하유신 ( Ha U-Syn ) - Catholic University College of Medicine Department of Urology
홍성후 ( Hong Sung-Hoo ) - Catholic University College of Medicine Department of Urology
이지열 ( Lee Ji-Youl ) - Catholic University College of Medicine Department of Urology
문명건 ( Moon Myeong-Keon ) - Buheung Medical
문성희 ( Moon Sung-Hee ) - Buheung Medical
김세웅 ( Kim Sae-Woong ) - Catholic University College of Medicine Department of Urology
배웅진 ( Bae Woong-Jin ) - Catholic University College of Medicine Department of Urology

Abstract


Purpose: Chronic prostatitis (CP), including chronic pelvic pain syndrome (CPPS), is the most commonly encountered manifestation of prostatitis. The aim of this study was to evaluate the effect of electric stimulation hyperthermia treatment (ESHT) on CP/CPPS and to explore the underlying mechanism.

Materials and Methods: RWPE-2 cells with lipopolysaccharide-induced inflammation and a prostatitis rat model induced by 17β-estradiol and dihydrotestosterone underwent sham, electric stimulation, or ESHT treatment. Four weeks later, cells, supernatants, and rat prostates were collected for analysis using immunohistochemistry, Western blots, and enzyme-linked immunosorbent assays.

Results: We found that ESHT improved prostatitis in vivo and attenuated inflammation in vitro. ESHT significantly induced suppressor of cytokine signaling 3 (SOCS3) expression and subsequently promoted HSP70. It attenuated inflammation through decreased expression of toll-like receptor 4 (TLR4), nuclear factor kappa B, and subsequent inflammatory cytokines. ESHT also inhibited apoptosis and released growth factor in tissue affected by prostatitis.

Conclusions: ESHT improved CP/CPPS and reversed pathologic changes of prostatitis by inhibiting the SOCS3-TLR4 pathway.

키워드

Electric stimulation hyperthermia treatment; Neuroinflammation; Prostatitis; Suppressor of cytokine signaling 3-toll like receptor 4 pathway

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