辣椒素受体介导氯喹引起的搔痒

目的研究辣椒素受体（VR1）在氯喹引起搔痒中的作用及机制。方法实验分4个部分，分别研究辣椒素受体拮抗剂辣椒平腹腔注射、局部应用辣椒素使VR1脱敏感、局部注射PKA抑制剂H89或PKC抑制剂bisindolylmaleimide Ⅰ、重复肥大细胞脱颗粒后颈背部注射氯喹200μg／100μl 30min内引起搔痒的次数，分为9小组，共使用6周龄C57BL／6J雄性小鼠63只。结果腹腔内注射辣椒平、局部应用辣椒素与重复肥大细胞脱颗粒均明显抑制氯喹引起的搔痒，而H89与BIM对氯喹引起的搔痒均无明显作用。结论氯喹通过肥大细胞脱颗粒引起搔痒，而辣椒素受体介导了氯喹引起的搔痒。

Role of Vanilloid Receptor in Chloroquine-lnduced Pruritus

Objective To evaluate the role of vanilloid receptor in chloroquine-induced pruritus. Methods Four groups of experiment were performed to study the effects of （1） peritoneal injection of capsazepine （vanilloid receptor antagonist）, （2） topical application of capsaicin for desensitization of VR1, （3） local injection of H89 （PKA inhibitor） or bisindolylmaleimide Ⅰ （PKC inhibitor） and （4） repeated mast cell degranulation on pruritus induced by intradermal injection with chloroquine to the rostral part of the neck. A total of sixty three C57BL/6J mice were divided into 9 groups. Results Scratching behavior after chloroquine injection was decreased in mice receiving peritoneal injection of capsazepine, topical capsaicin and repeated mast cell degranulation, but not by H89 or bisindolylmaleimide Ⅰ. Conclusion Chloroquine-induced pruritus is due to VRl-mediated mast cell degranulation.