Endogenous
cannabinoids and peripheral
cannabinoid CB2 receptors (CB2Rs) are involved in the antinociceptive effect of
electroacupuncture (EA) on inflammatory
pain. However, it is not clear how CB2R activation contributes to the antinociceptive effect of EA. The major proinflammatory
cytokines, such as tumour
necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and
IL-6, are involved in inflammatory
pain. Here we determined the effects of CB2R activation and EA on the expression level of IL-1β,
IL-6 and TNF-α in inflamed skin tissues. Inflammatory
pain was induced by injection of complete
Freund's adjuvant into the left hindpaw of rats.
Thermal hyperalgesia was tested with a radiant heat stimulus, and
mechanical allodynia was quantified using von Frey filaments. The
mRNA and
protein levels of IL-1β,
IL-6 and TNF-α in inflamed skin tissues were measured using real-time polymerase chain reaction and Western blot, respectively. Local injection of the selective CB2R agonist
AM1241 or EA applied to GB30 and GB34 significantly reduced
thermal hyperalgesia and
mechanical allodynia induced by tissue
inflammation. The specific CB2R antagonist
AM630 significantly attenuated the antinociceptive effect of EA. Furthermore, EA or
AM1241 treatment significantly decreased the
mRNA and
protein levels of IL-1β,
IL-6 and TNF-α in inflamed skin tissues. In addition, pretreatment with
AM630 significantly reversed the inhibitory effect of EA on these
cytokine levels in inflamed skin tissues. Our results suggest that EA reduces inflammatory
pain and proinflammatory
cytokines in inflamed skin tissues through activation of CB2Rs.