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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/100μ l30min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。
Objective To investigate the role and mechanism of capsaicin receptor (VR1) in pruritus induced by chloroquine. Methods The experiment was divided into four parts. The capsaicin receptor antagonist pepper was intraperitoneally injected. The capsaicin was applied locally to desensitize the VR1. The PKA inhibitor H89 or bisindolylmaleimide I was injected locally. The mast cells were degranulated and then dorsomedrally The number of pruritus caused by injection of chloroquine 200 μg / 100 μL for 30 min was divided into 9 groups of 63 C57BL / 6J male mice of 6 weeks old. Results Intraperitoneal injection of capsaicin, topical application of capsaicin and repeated mast cell degranulation significantly inhibited the pruritus caused by chloroquine, while H89 and BIM had no significant effect on chloroquine-induced pruritus. Conclusion Chloroquine induced pruritus by degranulation of mast cells, whereas capsaicin receptor mediated pruritus caused by chloroquine.