Abstract
Neuropathic pain in a chronic post-ischaemic pain (CPIP) model mimics the symptoms of complex regional pain syndrome type I (CRPS I). The administration of bee venom (BV) has been utilized in Eastern medicine to treat chronic inflammatory diseases accompanying pain. However, the analgesic effect of BV in a CPIP model remains unknown. The application of a tight-fitting O-ring around the left ankle for a period of 3 h generated CPIP in C57/Bl6 male adult mice. BV (1 mg/kg; 1, 2, and 3 times) was administered into the SC layer of the hind paw, and the antiallodynic effects were investigated using the von Frey test and by measuring the expression of neurokinin type 1 (NK-1) receptors in dorsal root ganglia (DRG). The administration of BV dose-dependently reduced the pain withdrawal threshold to mechanical stimuli compared with the pre-administration value and with that of the control group. After the development of the CPIP model, the expression of NK-1 receptors in DRG increased and then decreased following the administration of BV. SC administration of BV results in the attenuation of allodynia in a mouse model of CPIP. The antiallodynic effect was objectively proven through a reduction in the increased expression of NK-1 receptors in DRG.
Highlights
Bee venom (BV) has been used in traditional eastern medicine to relieve pain and to treat chronic inflammatory diseases
Our findings reveal that a novel animal model of complex regional pain syndrome type I
(CRPS I), a chronic post-ischaemic pain (CPIP) model, developed mechanical allodynia, which was attenuated by the administration of bee venom (BV)
Summary
Bee venom (BV) has been used in traditional eastern medicine to relieve pain and to treat chronic inflammatory diseases. Various studies have demonstrated the analgesic and anti-inflammatory, as well as anti-cancer, effects of BV. BV contains various peptides, amines, nonpeptide components, and free amino acids, which are presumed to have anti-inflammatory, analgesic, and anti-cancer effects. Recent studies have revealed diverse mechanisms underlying the analgesic and anti-inflammatory effects of BV. (COX-2) and phospholipase A2 (PLA2), in addition to the generation of mediators such as tumour necrosis factor-α (TNF-α), interleukin (IL)-1, IL-6, nitric oxide (NO), and reactive oxygen species (ROS), have been reported to be related to the analgesic and anti-arthritic effects of BV [1,2,3]. Previous studies have demonstrated that BV treatment has analgesic effects in neuropathic pain animal models, with possible mechanisms including the activation of alpha 2-adrenoceptors, the reduction in c-Fos
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