Suppressive Effects of Bee Venom Acupuncture on Paclitaxel-Induced Neuropathic Pain in Rats: Mediation by Spinal α₂-Adrenergic Receptor

Paclitaxel, a chemotherapy drug for solid tumors, induces peripheral painful neuropathy. Bee venom acupuncture (BVA) has been reported to have potent analgesic effects, which are known to be mediated by activation of spinal α-adrenergic receptor. Here, we investigated the effect of BVA on mechanical...

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Bibliographic Details
Published in:Toxins 2017-10, Vol.9 (11), p.351
Main Authors: Choi, Jiho, Jeon, Changhoon, Lee, Ji Hwan, Jang, Jo Ung, Quan, Fu Shi, Lee, Kyungjin, Kim, Woojin, Kim, Sun Kwang
Format: Article
Language:English
Subjects:
Acupuncture
Adrenergic receptors
Analgesics
bee venom acupuncture
Chemotherapy
chemotherapy-induced neuropathic pain
Hyperalgesia
Paclitaxel
Pain
Pain perception
Peripheral neuropathy
Phospholipase
Phospholipase A2
Prazosin
Pretreatment
Rats
Rodents
Solid tumors
Venom
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Summary:Paclitaxel, a chemotherapy drug for solid tumors, induces peripheral painful neuropathy. Bee venom acupuncture (BVA) has been reported to have potent analgesic effects, which are known to be mediated by activation of spinal α-adrenergic receptor. Here, we investigated the effect of BVA on mechanical hyperalgesia and spinal neuronal hyperexcitation induced by paclitaxel. The role of spinal α-adrenergic receptor subtypes in the analgesic effect of BVA was also observed. Administration of paclitaxel (total 8 mg/kg, intraperitoneal) on four alternate days (days 0, 2, 4, and 6) induced significant mechanical hyperalgesic signs, measured using a von Frey filament. BVA (1 mg/kg, ST36) relieved this mechanical hyperalgesia for at least two hours, and suppressed the hyperexcitation in spinal wide dynamic range neurons evoked by press or pinch stimulation. Both melittin (0.5 mg/kg, ST36) and phospholipase A2 (0.12 mg/kg, ST36) were shown to play an important part in this analgesic effect of the BVA, as they significantly attenuated the pain. Intrathecal pretreatment with the α₂-adrenergic receptor antagonist (idazoxan, 50 µg), but not α₁-adrenergic receptor antagonist (prazosin, 30 µg), blocked the analgesic effect of BVA. These results suggest that BVA has potent suppressive effects against paclitaxel-induced neuropathic pain, which were mediated by spinal α₂-adrenergic receptor.
ISSN:2072-6651
2072-6651
DOI:10.3390/toxins9110351