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电刺激热疗通过细胞因子信号转导抑制因子3- Toll样受体4通路减轻前列腺炎大鼠模型的炎症

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

作者信息

Zhu Guan Qun, Jeon Seung Hwan, Lee Kyu Won, Tian Wen Jie, Cho Hyuk Jin, Ha U Syn, Hong Sung Hoo, Lee Ji Youl, Moon Myeong Keon, Moon Sung Hee, Kim Sae Woong, Bae Woong Jin

机构信息

Department of Urology, College of Medicine, The Catholic University of Korea, Seoul, Korea.

Catholic Integrative Medicine Research Institute, The Catholic University of Korea, Seoul, Korea.

出版信息

World J Mens Health. 2020 Jul;38(3):359-369. doi: 10.5534/wjmh.190078. Epub 2019 Jul 23.

DOI:10.5534/wjmh.190078
PMID:31385476
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7308236/
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 and attenuated inflammation . 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.

摘要

目的

慢性前列腺炎(CP),包括慢性盆腔疼痛综合征(CPPS),是前列腺炎最常见的表现形式。本研究旨在评估电热疗法(ESHT)对CP/CPPS的疗效,并探讨其潜在机制。

材料与方法

用脂多糖诱导RWPE - 2细胞发生炎症,并采用17β - 雌二醇和二氢睾酮诱导建立前列腺炎大鼠模型,分别进行假手术、电刺激或ESHT治疗。四周后,收集细胞、上清液和大鼠前列腺,采用免疫组织化学、蛋白质免疫印迹法和酶联免疫吸附测定法进行分析。

结果

我们发现ESHT改善了前列腺炎并减轻了炎症。ESHT显著诱导细胞因子信号转导抑制因子3(SOCS3)表达,随后促进热休克蛋白70(HSP70)表达。它通过降低Toll样受体4(TLR4)、核因子κB及后续炎性细胞因子的表达来减轻炎症。ESHT还抑制了前列腺炎病变组织中的细胞凋亡并释放生长因子。

结论

ESHT通过抑制SOCS3 - TLR4途径改善了CP/CPPS并逆转了前列腺炎的病理变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d68/7308236/ab51ce855654/wjmh-38-359-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d68/7308236/9377f2435db0/wjmh-38-359-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d68/7308236/55e55e05bcb5/wjmh-38-359-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d68/7308236/48dec8874dc7/wjmh-38-359-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d68/7308236/ab51ce855654/wjmh-38-359-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d68/7308236/9377f2435db0/wjmh-38-359-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d68/7308236/9aafce8eabf2/wjmh-38-359-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d68/7308236/55e55e05bcb5/wjmh-38-359-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d68/7308236/48dec8874dc7/wjmh-38-359-g005.jpg
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