TRPV1 Responses in the Cerebellum Lobules V, VIa and VII Using Electroacupuncture Treatment for Inflammatory Hyperalgesia in Murine Model

• Published in: International journal of molecular sciences Vol. 21; no. 9; p. 3312
• Main Authors: Inprasit, Chanya, Lin, Yi-Wen
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 07-05-2020; MDPI
• Subjects: Acupuncture; Acupuncture Points; Analgesics; Animal models; Animals; Brain research; Capsaicin receptors; Cerebellum; Cerebellum - metabolism; Disease Models, Animal; Electroacupuncture; Electroacupuncture - methods; Freund's Adjuvant - adverse effects; Gene Expression Regulation; Hyperalgesia; Hyperalgesia - genetics; Hyperalgesia - immunology; Hyperalgesia - therapy; Immunoblotting; Immunofluorescence; Inflammation; inflammatory pain; Kinases; Male; MAP Kinase Signaling System; Medical research; Mice; Narcotics; Pain; Pain perception; Physiology; Proteins; Signal Transduction; ST36; Treatment Outcome; TRPV Cation Channels - genetics; TRPV Cation Channels - metabolism; TRPV1; inflammatory pain; ST36; TRPV1; electroacupuncture; cerebellum
• ISSN: 1422-0067; 1661-6596; 1422-0067
• 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.