解毒活血汤通过激活Wnt/GSKβ/β-连环蛋白信号通路和减轻细胞凋亡来改善慢性非细菌性前列腺炎/慢性盆腔疼痛综合征。

Jiedu Huoxue decoction improves chronic abacterial prostatitis/chronic pelvic pain syndrome through activating Wnt/GSKβ/β-catenin signaling pathway and alleviating apoptosis.

作者信息

Yi Jun, Pan Junqing, Zhang Sina, Mao Wenli, Wang Jiangang, Wang Wanchun, Yan Zhangren

机构信息

Department of Traditional Chinese Medicine Surgery, Affiliated Hospital of Jiangxi University of Chinese Medicine, No.445 Bayi Avenue, Nanchang 330006, China.

出版信息

Biomed Pharmacother. 2022 May;149:112830. doi: 10.1016/j.biopha.2022.112830. Epub 2022 Mar 17.

DOI:10.1016/j.biopha.2022.112830

PMID:35306428

Abstract

BACKGROUND

Chronic abacterial prostatitis/chronic pelvic pain syndrome (CP/CPPS) accounts for 90% of clinical prostatitis, and there is no specific and effective treatment for it. Jiedu Huoxue decoction (JDHXD) has been believed to be an effective agent for CP/CPPS, but the specific mechanism remains unclear.

METHODS

Carrageenan and LPS were used to established the animal and cell models of CP/CPPS, respectively. The prostate index, urine volume, lumen area, epithelial thickness, and pain response time were investigated. TUNEL staining and flow cytometry were applied to measure apoptosis levels in vivo and in vitro.

RESULTS

JDHXD improved CP/CPPS recovery in a dose-dependent manner. JDHXD restrained apoptosis and activated Wnt/GSK-3β/β-catenin signaling pathway in the CP/CPPS animal model. Inhibition of Wnt/GSK-3β/β-catenin signaling pathway remarkably aggravated apoptosis and suppressed the improvement of CP/CPPS by JDHXD. XAX939 markedly reversed the suppression of cell apoptosis and ROS level caused by JDHXD in vitro.

CONCLUSION

Jiedu Huoxue decoction improved CP/CPPS through activating Wnt/GSKβ/β-catenin signaling pathway and inhibiting apoptosis. This study might provide a novel insight for the prevention and treatment of CP/CPPS through activating Wnt/GSK-3β/β-catenin signaling pathway.

摘要

背景

慢性非细菌性前列腺炎/慢性盆腔疼痛综合征（CP/CPPS）占临床前列腺炎的90%，且尚无特异性有效的治疗方法。解毒活血汤（JDHXD）被认为是治疗CP/CPPS的有效药物，但其具体机制尚不清楚。

方法

分别用角叉菜胶和脂多糖建立CP/CPPS的动物和细胞模型。研究前列腺指数、尿量、管腔面积、上皮厚度和疼痛反应时间。采用TUNEL染色和流式细胞术检测体内外凋亡水平。

结果

JDHXD以剂量依赖方式改善CP/CPPS的恢复。JDHXD抑制CP/CPPS动物模型中的细胞凋亡并激活Wnt/GSK-3β/β-连环蛋白信号通路。抑制Wnt/GSK-3β/β-连环蛋白信号通路显著加重细胞凋亡，并抑制JDHXD对CP/CPPS的改善作用。XAX939显著逆转了JDHXD在体外对细胞凋亡和活性氧水平的抑制作用。