电针刺激中鸡(CV3)、关原(CV4)和双侧大河(KI12)通过抑制toll样受体4途径减轻雌二醇诱导的慢性非细菌性前列腺炎大鼠的炎症反应。

L I Zhihao, Han Wenjun, Song Xiuling, L I Yan, Chen Yuelai
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引用次数: 0

摘要

目的:探讨电针对慢性前列腺炎/慢性盆腔疼痛综合征(CP/CPPS)(也称为慢性非细菌性前列腺炎(CNP))的抗炎作用,并探讨其潜在机制。方法:雄性Sprague-Dawley大鼠采用手术去势联合注射17-β雌二醇连续30天建立CNP大鼠模型。CNP大鼠接受电针治疗,每天一次,持续8天。慢性盆腔疼痛通过机械戒断阈值测量进行评估。苏木精-伊红染色评估组织学变化。用酶联免疫吸附法测定前列腺中的炎性细胞因子。免疫印迹法检测toll样受体4(TLR4)、骨髓分化因子88(MyD88)、κBα抑制剂(IκBα)和核因子κB(NF-κB)的表达。免疫荧光染色观察NF-κB的核转位和TLR4的定位。结果:电针降低前列腺指数,上调机械戒断阈值,恢复前列腺组织形态,降低炎症因子水平,抑制NF-κB p65核转位,下调参与TLR4/NF-κB信号通路的关键蛋白在前列腺中的表达水平。结论:电针可减轻雌二醇诱导的CNP大鼠盆腔疼痛,减轻前列腺炎症。其潜在机制可能与TLR4/NF-κB信号通路的抑制有关。
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Electroacupuncture stimulating Zhongji (CV3), Guanyuan (CV4), and bilateral Dahe (KI12) attenuates inflammation in rats with chronic nonbacterial prostatitis induced by estradiol through inhibiting toll-like receptor 4 pathway.

Objective: To investigate the anti-inflammatory effect of electroacupuncture (EA) on chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), also known as chronic nonbacterial prostatitis (CNP), and explore its underlying mechanism.

Methods: A CNP rat was established by surgical castration combined with 17-β estradiol injection in male Sprague-Dawley rats for thirty consecutive days. The CNP rats received EA treatment once a day for eight days. Chronic pelvic pain was evaluated by mechanical withdrawal threshold measurement. The histological change was assessed by hematoxylin-eosin staining. The inflammatory cytokines in prostates were determined by enzyme-linked immunosorbent assays. The expressions of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), inhibitors of kappa-B alpha (IκBα), and nuclear factor-kappa B (NF-κB) were detected by Western blotting. The nuclear translocation of NF-κB and the location of TLR4 were observed with immunofluorescence staining.

Results: The results showed that EA decreased the prostate index, upregulated the mechanical withdrawal threshold, restored the histomorphology of the prostate, reduced the inflammatory factor levels, inhibited NF-κB p65 nuclear translocation, and downregulated the expression levels of critical proteins involved in the TLR4/NF-κB signaling pathway in prostates.

Conclusions: Our findings suggested that EA could relieve pelvic pain and attenuate prostatic inflammation in estradiol-induced CNP rats. The underlying mechanism may be related to the inhibition of the TLR4/NF-κB signaling pathway.

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