Antiallodynic Effects of Bee Venom in an Animal Model of Complex Regional Pain Syndrome Type 1 (CRPS-I)

被引:8
|
作者
Lee, Sung Hyun [1 ]
Lee, Jae Min [2 ]
Kim, Yun Hong [1 ]
Choi, Jung Hyun [2 ]
Jeon, Seung Hwan [3 ]
Kim, Dong Kyu [2 ]
Jeong, Hyeon Do [2 ]
Lee, You Jung [2 ]
Park, Hue Jung [2 ]
机构
[1] Sungkyunkwan Univ, Kangbuk Samsung Hosp, Dept Anesthesiol & Pain Med, Sch Med, Seoul 03181, South Korea
[2] Catholic Univ Korea, Seoul St Marys Hosp, Dept Anesthesiol & Pain Med, Coll Med, Seoul 06591, South Korea
[3] Catholic Univ Korea, Seoul St Marys Hosp, Dept Urol, Coll Med, Seoul 06591, South Korea
来源
TOXINS | 2017年 / 9卷 / 09期
关键词
allodynia; bee venom; chronic post-ischaemic pain; complex regional pain syndrome; SUBSTANCE-P; ACUPUNCTURE; EXPRESSION; ALLODYNIA;
D O I
10.3390/toxins9090285
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
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.
引用
收藏
页数:9
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