Research progress on the role of oxidative stress signaling pathways in pain pathogenesis of chronic prostatitis/chronic pelvic pain syndrome
张强 1苏旭珍 1项瑞君 1张春雷 2张斌 2常德辉2
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作者信息
1. 甘肃中医药大学 临床医学院,甘肃 兰州 730030
2. 解放军联勤保障部队第九四〇医院 泌尿外科,甘肃 兰州 730050
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摘要
慢性前列腺炎/慢性盆腔疼痛综合征(chronic prostatitis/chronic pelvic pain syndrome,CP/CPPS)是泌尿外科常见疾病.在CP/CPPS治疗研究进展中,发现通过核因子-κB(nuclear factor-kappa B,NF-κB)、核因子E2相关因子2(nuclear factor erythroid 2-related factor 2,Nrf2)、丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)等信号通路联合调控氧化应激和炎症反应,可减轻CP/CPPS症状.近年来,发现通过调控叉头盒转录因子(forkhead box O,FOXO)、沉默信息调节因子1(silent information regulator 1,Sirt1)、外来信号调节激酶(extracellular signal-regulated kinase,Erk)、GTP酶动力蛋白家族(ras homolog gene family member A,RhoA)/Rho相关蛋白激酶1(Rho-associated protein kinase 1,ROCK1)等信号通路,来缓解前列腺炎症和盆腔疼痛,为CP/CPPS的治疗提供新的靶点.
Abstract
Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common urological disease.In the research progress of CP/CPPS treatment,it has been found that the regulation of oxidative stress and inflammation response through nuclear factor kappa-B (NF-κB),nuclear factor erythroid-2 related factor 2 (Nrf2),mitogen-activated protein kinase (MAPK) and other signaling pathways can reduce CP/CPPS symptoms.In recent years,it has been found that the regulation of forkhead box O (FOXO),silent information regulator 1(Sirt1),extracellular signal-regulated kinase(Erk),ras homolog gene family member A(RhoA)/Rho-associated protein kinase 1(ROCK1) and other signaling pathways can relieve prostatic inflammation and pelvic pain,providing a new target for CP/CPPS treatment.
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