The anti-nociceptive effect and the possible mechanism of acupoint stimulation caused by chemical irritants in the bee venom pain model

Abstract

Many studies have demonstrated the anti-nociceptive and anti-inflammatory effects of injecting bee venom (BV) into the Zusanli (ZSL) acupoint in rats. The present study was designed to determine whether the injection of other chemical irritants, such as formalin and complete Freund's adjuvant (CFA), into the ZSL acupoint can produce anti-nociceptive and anti-inflammatory effects in the BV pain model and to determine the possible mechanisms underlying these effects. First, the effects of injecting BV, formalin, CFA, or saline into the ZSL acupoint on intraplantar BV-induced persistent spontaneous pain, mechanical hyperalgesia, and inflammatory swelling of the injected paw were observed. BV, formalin, CFA, and saline injection into the ZSL acupoint significantly inhibited intraplantar BV-induced persistent spontaneous nociception (PSN) and mechanical hyperalgesia but had no effect on intraplantar BV-induced inflammatory swelling. Next, the effects of pretreatment with naloxone (5 mg/kg, ip) or injection of 0.15% capsaicin into the ZSL acupoint on the anti-nociceptive effect of BV acupuncture (BVA) were observed. Pretreatment with naloxone had no effect on the BVA-induced anti-nociceptive effect, intraplantar BV-induced PSN, and mechanical hyperalgesia. Pretreatment with capsaicin produced partial blockage of the BVA-induced anti-nociceptive effect on PSN, but it had no effect on BVA-induced anti-nociception of mechanical hyperalgesia. These results suggest that (1) chemical irritant acupuncture produces the anti-nociceptive effect but not the anti-inflammatory effect in the BV pain model, and (2) chemical irritant acupuncture-induced analgesia is a common mechanism that is not specific to BV acupuncture. Our results also suggest that the BVA-induced anti-nociceptive mechanism is partially mediated by capsaicin-sensitive primary afferent fibers but not by endogenous mu opioid receptors in the BV pain model.