摘要
目的研究蛋白激酶C(PKC)途径在内皮素-1(ET-1)引起热痛觉过敏中的作用。方法小鼠分为PKC抑制剂BisindolylmaleimideⅠ(BIM)组(BIM组)、ET-1组(ET组)、BIM加ET-1组(BE组),每组6只。BIM组足底注射BIM5nmol15min后再注射PBS,ET-1组注射PBS15min后再注射10pmolET-1,BE组注射5nmolBIM15min后再注射10pmolET-1。测量注药前及注药后15、30、45及60min对热逃避反应时间。结果BIM组与BE组热痛觉阈值无明显变化,ET组热痛觉阈值降低。结论局部注射ET-1通过激活PKC途径从而引起热痛觉过敏。
Objective To evaluate the role of protein kinase C （PKC） in the thermal hyperalgesia evoked by local injection of endothelin-1 （ET-1）. Method C57BL/6 mice were divided into BIM group （intraplantar injection of 5nmol of PKC inhibitor Bisindolylmaleimide I followed by PBS injection 15 min later）, ET group （intraplantar injection of PBS injection followed by 10 pmol of ET-1 injection）, and BE group （intraplantar injection of 5nmol of PKC inhibitor Bisindolylmaleimide I followed by 10 pmol of ET-1 injection）. （Six in each group）. A volume of 10 μl was used in each injection. And latency time of paw withdrawal from irradiation heat stimulation was measured before injection and 15 min, 30 min, 45 min, 60 min after tperalgesia via activation of protein kinase C pathway. Result Pretreatmeat with BIM completely inhibited thermal hyperalgesia induced by ET-1. And prior injection of PBS didn＇t show any influence on thermal hyperalgesia induced by ET-1. Conclusion Peripheral ET-1 produces thermal hyperalgesia via activation of protein kinase C pathway.
出处
《热带医学杂志》
CAS
2006年第12期1293-1294,1276,共3页
Journal of Tropical Medicine
