目的·观察蛋白酶激活受体2（protease activated receptor 2, PAR2）对糖尿病小鼠结肠运动的影响，并探究其作用机制。方法·通过腹腔注射链脲佐菌素构建小鼠1型糖尿病模型。分离小鼠结肠平滑肌和肠段，通过肌条张力收缩实验和结肠移行性复合运动实验，观察PAR2激动剂对结肠运动的作用，以及小电导钙激活钾通道(small conductance calcium-activated potassium channel, SK3通道)阻断剂对其作用的影响。结果·PAR2受体激动剂对糖尿病小鼠结肠平滑肌运动的抑制作用较正常小鼠明显增强，SK3通道阻断剂可以抑制PAR2受体激动剂的作用。结论·糖尿病小鼠结肠中PAR2功能亢进，PAR2可能通过SK3通道抑制结肠运动。

Objective · To observe the effect of protease activated receptor 2 (PAR2) on the colonic motility in diabetic mice and investigate the mechanism. Methods · The momodel of type 1 diabetes mellitus was establishedintraperitoneal injection of streptozotocin. The smooth muscle strips and segments of colons were isolated. The effects of PAR2 agonist on colonic motility were observedmuscle strip tension contraction and colonic migrating motor complex experiments. The effect of small conductance calcium-activated potassium channel (SK3 channel) antagonist on it was also observed. Results · PAR2 agonist inhibited colonic motility and colonic smooth muscle was more sensitive to PAR2 agonist in diabetic mice. PAR2 agonist-induced inhibition was inhibitedSK3 channel antagonist. Conclusion · PAR2 activity in diabetic mice colons is significantly enhanced, which may inhibit colonic motility through SK3 channel.