Wu Xiao-Ling, Cheng Kai, Xu Chang, Chai Ye-Mao, Yap Tai-Heng, Yang Zhi-Wen, Sun Qian-Hui, Tan Yan, Zhang Jia-Ni, Chen Wei, Qiu Xing-Hua, Yang Xing-Yue, Li Na
College of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, China.
College of Academy of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
Front Neurosci. 2022 Aug 24;16:938200. doi: 10.3389/fnins.2022.938200. eCollection 2022.
To investigate the analgesic mechanism of electroacupuncture (EA) in rats with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS).
Thirty male SD rats were randomly divided into sham group, model group and EA group, with ten rats in each group. The CP/CPPS model was prepared by injecting 50 μL of complete Freund's adjuvant (CFA) into the ventral lobes of the prostate tissue, and the sham group was injected with the same dose of saline. After 14 days of modeling, EA was applied to Guanyuan (CV4), Zhongji (CV3), Sanyinjiao (SP6) and Huiyang (BL35) in the EA group. After four courses, H&E staining was performed to observe the prostate tissue morphology, transcriptome sequencing (RNA-Seq) was performed for each group, and the selected signaling pathways were verified by qRT-PCR.
The RNA-Seq analysis results suggested that the analgesic effect of EA on CP/CPPS may be achieved by regulating prostate gene expression, which may be related to multiple biological processes and signaling pathways. qRT-PCR results showed that the vanillic acid receptor subtype 1 of the transient receptor potential (TRPV1), phospholipase C (PLC), protein kinase C (PKC), cyclic adenosine monophosphate (cAMP), and protein kinase A (PKA) were all upregulated in the model group compared to the sham group ( < 0.01). Compared with the model group, TRPV1, PLC, PKC, cAMP, and PKA were all downregulated in the EA group ( < 0.05, < 0.01).
The analgesic mechanism of EA on CP/CPPS may be achieved through modulation of cAMP-PKA-TRPV1/PLC-PKC-TRPV1 signaling pathway.
探讨电针(EA)对慢性前列腺炎/慢性盆腔疼痛综合征(CP/CPPS)大鼠的镇痛机制。
30只雄性SD大鼠随机分为假手术组、模型组和电针组,每组10只。通过向前列腺组织腹叶注射50 μL完全弗氏佐剂(CFA)制备CP/CPPS模型,假手术组注射相同剂量的生理盐水。造模14天后,电针组针刺关元(CV4)、中极(CV3)、三阴交(SP6)和会阳(BL35)。经过四个疗程后,进行苏木精-伊红(H&E)染色观察前列腺组织形态,对每组进行转录组测序(RNA-Seq),并通过实时定量聚合酶链反应(qRT-PCR)验证所选信号通路。
RNA-Seq分析结果表明,电针对CP/CPPS的镇痛作用可能是通过调节前列腺基因表达实现的,这可能与多个生物学过程和信号通路有关。qRT-PCR结果显示,与假手术组相比,模型组瞬时受体电位香草酸受体1型(TRPV1)(瞬时受体电位)、磷脂酶C(PLC)、蛋白激酶C(PKC)、环磷酸腺苷(cAMP)和蛋白激酶A(PKA)均上调(<0.01)。与模型组相比,电针组TRPV1、PLC、PKC、cAMP和PKA均下调(<0.05,<0.01)。
电针对CP/CPPS的镇痛机制可能是通过调节cAMP-PKA-TRPV1/PLC-PKC-TRPV1信号通路实现的。