College of Chinese Medicine, Graduate Institute of Acupuncture Science, China Medical University, Taichung 40402, Taiwan.
Chinese Medicine Research Center, China Medical University, Taichung 40402, Taiwan.
Int J Mol Sci. 2020 May 7;21(9):3312. doi: 10.3390/ijms21093312.
Inflammatory pain sensation is an important symptom which protects the body against additional tissue damage and promotes healing. Discovering long-term and effective treatments for pain remains crucial in providing efficient healthcare. Electroacupuncture (EA) is a successful therapy used for pain relief. We aimed to investigate effects and mechanisms of Complete Freund's Adjuvant (CFA)-inducing inflammatory pain in the cerebellum, and the inhibition of this inflammatory hyperalgesia using EA at Zusanli acupoint (ST36). The results display a significant increase in mechanical and thermal sensitivities in the CFA and CFA + SHAM groups, which was significantly reduced in the CFA+EA and CFA + KO groups. This evidence was substantiated in the protein levels observed using immunoblotting, and presented with significant escalations after CFA inducing inflammatory hyperalgesia in CFA and CFA + SHAM groups. Then, they were significantly attenuated by EA in the CFA + EA group. Furthermore, the CFA + transient receptor vanilloid member 1 (TRPV1) group indicated similar significant decreases of protein expression. Additionally, a concomitant overexpression in lobule VIa was also observed in immunofluorescence. These consequences suggest that CFA-induced inflammatory pain provokes modifications in cerebellum lobules V, VIa and VII, which can subsequently be regulated by EA treatment at the ST36 through its action on TRPV1 and related molecular pathways.
炎性疼痛感觉是一种重要的症状,可保护身体免受进一步的组织损伤并促进愈合。发现长期有效的疼痛治疗方法对于提供有效的医疗保健仍然至关重要。电针(EA)是一种成功的治疗疼痛的方法。我们旨在研究完全弗氏佐剂(CFA)诱导的小脑炎性疼痛的作用和机制,以及使用 ST36 穴位(足三里)的 EA 抑制这种炎症性痛觉过敏。结果显示,CFA 和 CFA+SHAM 组的机械和热敏感性显著增加,而 CFA+EA 和 CFA+KO 组则显著降低。这一证据在免疫印迹观察到的蛋白水平上得到了证实,并且在 CFA 诱导的 CFA 和 CFA+SHAM 组的炎症性痛觉过敏后,蛋白水平显著升高。然后,EA 在 CFA+EA 组中显著减弱了它们。此外,CFA+瞬时受体香草素成员 1(TRPV1)组也显示出蛋白表达的类似显著下降。此外,在免疫荧光中还观察到小叶 VIa 的伴随过表达。这些结果表明,CFA 诱导的炎性疼痛引起小脑小叶 V、VIa 和 VII 的改变,随后通过 ST36 处的 EA 治疗通过 TRPV1 及其相关分子途径进行调节。