Abstract
Acupuncture therapy is effective in relieving postoperative pain of neck surgery, but its underlying mechanisms remain largely unknown. This study, in the incisional neck pain rat model, was designed to explore whether the endocannabinoid receptor 1 (CB1) in the cervical spinal cord is involved in the analgesic effect of electroacupuncture (EA) or not.The incisional neck pain model was established by making a longitudinal incision and applied EA treatment of Futu (LI18), Hegu-Neiguan (LI4-PC6), or Zusanli-Yanglingquan (ST36-GB34) for pain relief. The results showed that EA LI18 and EA LI4-PC6 effectively relieve allodynia caused by neck incision, which was obviously better than EA ST34-GB34 (P < 0.05). After EA, the expression levels of CB1 mRNA at 4h in the EALI18 group, and 24 and 48h in both EALI18 and EALI4-PC6 groups, and those of CB1 protein at 4, 24, and 48h in the EALI18 group, and the immunoactivity of CB1 in both EALI18 and EALI4-PC6 groups at 4h were significantly upregulated in contrast to those of the model group (P < 0.05). EA of either acupoint group had no effect on the expression of CB2 protein (P > 0.05). Moreover, the antinociceptive effect of EA was reversed by AM251 (CB1 antagonist). Immunofluorescence dual staining showed that CB1 expressed in astrocytes in the superficial layer (laminae I and II) of dorsal horns of the cervical spinal cord. Therefore, the findings of this study revealed that upregulation of CB1 expression in the cervical spinal cord contributes to the analgesic effect of EA in incisional neck pain rats. The CB1 receptor expresses on astrocytes.
Highlights
Postsurgical pain is a common acute pain and frequently seen in many common operations, such as thyroid surgery, inguinal hernia repair, and breast and chest surgery
E endocannabinoid system, consisting of two main ligands N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), which are considered to be the main endogenous ligands of the two corresponding receptors: cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2), is one of the key endogenous systems for processing pain sensation. e CB1 is the prominent subtype in the central nervous system (CNS), including spinal cord, thalamus, periaqueductal grey (PAG), amygdala, and rostroventromedial medulla [12, 13] and exists in the dorsal root ganglion, at presynaptic sites throughout the peripheral system and CNS [14], whereas CB2 is found principally on immune cells
In order to verify the role of CB1 receptor in mediating EA analgesia, the rats were randomly divided into two groups, DMSO + EA and CB1 antagonist (AM251) + EA, which were further randomized into two subgroups: intraperitoneal injection(I.P.) and intrathecal injection (I.T.), with 12 rats in each subgroup. ree rats were excluded due to dyskinesia
Summary
Postsurgical pain is a common acute pain and frequently seen in many common operations, such as thyroid surgery, inguinal hernia repair, and breast and chest surgery. E CB1 is the prominent subtype in the central nervous system (CNS), including spinal cord, thalamus, periaqueductal grey (PAG), amygdala, and rostroventromedial medulla [12, 13] and exists in the dorsal root ganglion, at presynaptic sites throughout the peripheral system and CNS [14], whereas CB2 is found principally (but not exclusively) on immune cells Both of them participate in Evidence-Based Complementary and Alternative Medicine nociceptive processing [14]. Activation of spinal CB1 and upregulation of spinal CB1-ERK1/2 signaling could enhance the antinociceptive effect of EA in morphine-induced hyperalgesia rats [24] These outcomes have detailed the functions of CB1 and CB2 in mediating the analgesic effect of EA, their association with the effect of EA in inducing the reduction of incisional neck pain (INP) has not been reported. Erefore, this study was designed to select the appropriate acupoint with the best analgesic efficacy for INP, to observe the dynamic effect of EA on the expression of CB1 mRNA and protein in DHs of the cervical spinal cord, and at last, to verify the effect of CB1 in mediating EA-induced analgesic effect by intrathecal and intraperitoneal administration of CB1 antagonist
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