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

被引：11

作者：

Zhu, Guan Qun ^{[1
,2
]}

Jeon, Seung Hwan ^{[1
,2
]}

Lee, Kyu Won ^{[1
,2
]}

Tian, Wen Jie ^{[1
,2
]}

Cho, Hyuk Jin ^{[1
]}

Ha, U-Syn ^{[1
]}

Hong, Sung Hoo ^{[1
]}

Lee, Ji Youl ^{[1
]}

Moon, Myeong Keon ^{[3
]}

Moon, Sung Hee ^{[3
]}

Kim, Sae Woong ^{[1
,2
]}

Bae, Woong Jin ^{[1
,2
]}

机构：

[1] Catholic Univ Korea, Coll Med, Dept Urol, Seoul, South Korea

[2] Catholic Univ Korea, Catholic Integrat Med Res Inst, Seoul, South Korea

[3] Buheung Med, Seoul, South Korea

来源：

WORLD JOURNAL OF MENS HEALTH | 2020年 / 38卷 / 03期

基金：

新加坡国家研究基金会;

关键词：

Electric stimulation hyperthermia treatment; Neuroinflammation; Prostatitis; Suppressor of cytokine signaling 3-toll like receptor 4 pathway; PELVIC PAIN SYNDROME; FACTOR-BETA; MECHANISMS; INDUCTION; SECRETION;

D O I：

10.5534/wjmh.190078

中图分类号：

R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

摘要：

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 17 beta-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.

引用

页码：359 / 369

页数：11

共 26 条

[1] Suppressor of cytokine signaling (SOCS) proteins indirectly regulate toll-like receptor signaling in innate immune cells [J].