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Electroacupuncture Attenuates CFA-induced Inflammatory Pain by suppressing Nav1.8 through S100B, TRPV1, Opioid, and Adenosine Pathways in Mice

View Article: PubMed Central - PubMed

ABSTRACT

Pain is associated with several conditions, such as inflammation, that result from altered peripheral nerve properties. Electroacupuncture (EA) is a common Chinese clinical medical technology used for pain management. Using an inflammatory pain mouse model, we investigated the effects of EA on the regulation of neurons, microglia, and related molecules. Complete Freund’s adjuvant (CFA) injections produced a significant mechanical and thermal hyperalgesia that was reversed by EA or a transient receptor potential V1 (TRPV1) gene deletion. The expression of the astrocytic marker glial fibrillary acidic protein (GFAP), the microglial marker Iba-1, S100B, receptor for advanced glycation end-products (RAGE), TRPV1, and other related molecules was dramatically increased in the dorsal root ganglion (DRG) and spinal cord dorsal horn (SCDH) of CFA-treated mice. This effect was reversed by EA and TRPV1 gene deletion. In addition, endomorphin (EM) and N6-cyclopentyladenosine (CPA) administration reliably reduced mechanical and thermal hyperalgesia, thereby suggesting the involvement of opioid and adenosine receptors. Furthermore, blocking of opioid and adenosine A1 receptors reversed the analgesic effects of EA. Our study illustrates the substantial therapeutic effects of EA against inflammatory pain and provides a novel and detailed mechanism underlying EA-mediated analgesia via neuronal and non-neuronal pathways.

No MeSH data available.


Related in: MedlinePlus

Schematic illustration of neuronal and non-neuronal mechanisms in EA-mediated analgesia of CFA-induced inflammatory pain.Summary diagram of how astrocyte, glial cells, and TRPV1 is crucial for inflammatory pain and related mechanisms. Our results show that EA can reduce S100B release from non-neuronal cell. We also indicated that EA can trigger the release of opioid and adenosine receptors for relieving inflammatory pain through TRPV1 pathway.
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f10: Schematic illustration of neuronal and non-neuronal mechanisms in EA-mediated analgesia of CFA-induced inflammatory pain.Summary diagram of how astrocyte, glial cells, and TRPV1 is crucial for inflammatory pain and related mechanisms. Our results show that EA can reduce S100B release from non-neuronal cell. We also indicated that EA can trigger the release of opioid and adenosine receptors for relieving inflammatory pain through TRPV1 pathway.

Mentions: CFA induced mechanical and thermal hyperalgesia in mice. This effect was accompanied by the activation of astrocytes and glial cells, which then released the RAGE ligand S100B. Inflammation also activated TRPV1 and triggered a signaling pathway that activated nociceptive Nav channels. These phenomena were abolished by EA and deletion of the TRPV1 gene. We demonstrated that EA triggers the release of both endogenous opiates and adenosine to relieve inflammatory pain in mice. This study identified a potential TRPV1-mediated signaling mechanism (Fig. 10). Given the specific analgesic effect of EA on inflammatory hyperalgesia, TRPV1 antagonists could further translate into clinical efficacy for treating pain. Our findings offer insight for EA clinical trials in patients with inflammatory pain.


Electroacupuncture Attenuates CFA-induced Inflammatory Pain by suppressing Nav1.8 through S100B, TRPV1, Opioid, and Adenosine Pathways in Mice
Schematic illustration of neuronal and non-neuronal mechanisms in EA-mediated analgesia of CFA-induced inflammatory pain.Summary diagram of how astrocyte, glial cells, and TRPV1 is crucial for inflammatory pain and related mechanisms. Our results show that EA can reduce S100B release from non-neuronal cell. We also indicated that EA can trigger the release of opioid and adenosine receptors for relieving inflammatory pain through TRPV1 pathway.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5304170&req=5

f10: Schematic illustration of neuronal and non-neuronal mechanisms in EA-mediated analgesia of CFA-induced inflammatory pain.Summary diagram of how astrocyte, glial cells, and TRPV1 is crucial for inflammatory pain and related mechanisms. Our results show that EA can reduce S100B release from non-neuronal cell. We also indicated that EA can trigger the release of opioid and adenosine receptors for relieving inflammatory pain through TRPV1 pathway.
Mentions: CFA induced mechanical and thermal hyperalgesia in mice. This effect was accompanied by the activation of astrocytes and glial cells, which then released the RAGE ligand S100B. Inflammation also activated TRPV1 and triggered a signaling pathway that activated nociceptive Nav channels. These phenomena were abolished by EA and deletion of the TRPV1 gene. We demonstrated that EA triggers the release of both endogenous opiates and adenosine to relieve inflammatory pain in mice. This study identified a potential TRPV1-mediated signaling mechanism (Fig. 10). Given the specific analgesic effect of EA on inflammatory hyperalgesia, TRPV1 antagonists could further translate into clinical efficacy for treating pain. Our findings offer insight for EA clinical trials in patients with inflammatory pain.

View Article: PubMed Central - PubMed

ABSTRACT

Pain is associated with several conditions, such as inflammation, that result from altered peripheral nerve properties. Electroacupuncture (EA) is a common Chinese clinical medical technology used for pain management. Using an inflammatory pain mouse model, we investigated the effects of EA on the regulation of neurons, microglia, and related molecules. Complete Freund’s adjuvant (CFA) injections produced a significant mechanical and thermal hyperalgesia that was reversed by EA or a transient receptor potential V1 (TRPV1) gene deletion. The expression of the astrocytic marker glial fibrillary acidic protein (GFAP), the microglial marker Iba-1, S100B, receptor for advanced glycation end-products (RAGE), TRPV1, and other related molecules was dramatically increased in the dorsal root ganglion (DRG) and spinal cord dorsal horn (SCDH) of CFA-treated mice. This effect was reversed by EA and TRPV1 gene deletion. In addition, endomorphin (EM) and N6-cyclopentyladenosine (CPA) administration reliably reduced mechanical and thermal hyperalgesia, thereby suggesting the involvement of opioid and adenosine receptors. Furthermore, blocking of opioid and adenosine A1 receptors reversed the analgesic effects of EA. Our study illustrates the substantial therapeutic effects of EA against inflammatory pain and provides a novel and detailed mechanism underlying EA-mediated analgesia via neuronal and non-neuronal pathways.

No MeSH data available.


Related in: MedlinePlus