Abstract
Mas-related G-protein-coupled receptor C (MrgprC) plays an important role in modulating chronic inflammatory pain. Electroacupuncture (EA) has a satisfactory analgesic effect on chronic pain. This study aimed to investigate the involvement of MrgprC and its transient receptor potential vanilloid 1 (TRPV1) pathway in EA analgesia in chronic inflammatory pain. Chronic inflammatory pain was induced by subcutaneously injecting complete Freund's adjuvant (CFA) into the left hind paw. EA (2/100 Hz) stimulation was administered. MrgprC siRNAs were intrathecally administered to inhibit MrgprC expression, and bovine adrenal medulla 8-22 (BAM8-22) was used to activate MrgprC. The mechanical allodynia was decreased by EA significantly since day 3. The piled analgesic effect of EA was partially blocked by 6 intrathecal administrations of MrgprC siRNA. Both EA and BAM8-22 could downregulate the expression of TRPV1 and PKC in both the DRG and the SCDH. Both EA and BAM8-22 could also decrease the TRPV1 translocation and p-TRPV1 level in both the DRG and the SCDH. The effects of EA on PKCε, TRPV1 translocation, and p-TRPV1 in both the DRG and the SCDH were reversed by MrgprC siRNA. The results indicated that MrgprC played crucial roles in chronic pain modulation and was involved in EA analgesia partially through the regulation of TRPV1 function at the DRG and SCDH levels.
Highlights
Chronic inflammatory pain is a kind of refractory disease, and the prevalence rate in developing countries is higher than developed countries, with approximately 33% in the general adult population and 56% in the elderly population [1]
The results indicated that Mas-related G-protein-coupled receptor C (MrgprC) played crucial roles in chronic pain modulation and was involved in EA analgesia partially through the regulation of transient receptor potential vanilloid 1 (TRPV1) function at the dorsal root ganglia (DRG) and spinal cord dorsal horn (SCDH) levels
Considering our previous data [16, 36] showed that MrgprC expression in the DRG but not in the SCDH and bovine adrenal medulla 22 peptide (BAM22) release in both the DRG and the SCDH could be increased by EA in CFAinduced chronic inflammatory pain, the results indicated that MrgprC may play a role in modulation of EA over a 6day period of chronic inflammatory pain, and the possible analgesic mechanism of EA is associated with its upregulation on MrgprC in the DRG and activation of MrgprC by BAM22 in both the DRG and SCDH
Summary
Chronic inflammatory pain is a kind of refractory disease, and the prevalence rate in developing countries is higher than developed countries, with approximately 33% in the general adult population and 56% in the elderly population [1]. The ongoing input conveyed from peripheral neurons overexcites spinal nociceptive neurons, and central sensitization is induced. We found that local acupuncture can achieve better analgesic effects than distal acupuncture for treatment of chronic pain in clinics [6]. It is difficult to explain that local injection of anesthetic procaine showed inhibition of the EA analgesic effect [7]. A previous study showed that nociceptive response stimulated by complete Freund’s adjuvant (CFA) can be reduced by treatment with EA with dilatational 100 Hz and 2 Hz alternating frequencies (2/100 Hz) on ST36 [8], which is related to the peripheral endogenous opioid system [9]
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