A型肉毒毒素抑制乙酰胆碱诱发的大鼠离体幽门平滑肌的收缩

目的：观察A型肉毒毒素对内、外源性乙酰胆碱诱发的大鼠离体幽门平滑肌收缩的作用,并探讨其可能作用机制。方法：利用电场刺激诱发大鼠离体幽门平滑肌释放乙酰胆碱或加入外源性乙酰胆碱诱发肌条收缩,比较A型肉毒毒素与阿托品对该诱发收缩的作用。结果：A型肉毒毒素抑制电场刺激诱发的大鼠离体胃幽门平滑肌的收缩（P〈0.001）。阿托品和A型肉毒毒素均抑制乙酰胆碱诱发的大鼠离体胃幽门平滑肌的收缩（P〈0.001）,但A型肉毒毒素对乙酰胆碱诱发的收缩表现为不完全抑制。结论：A型肉毒毒素抑制电场刺激诱发内源性乙酰胆碱释放所产生的收缩作用,可能其裂解突触前膜上的SNAP-25蛋白而致;A型肉毒毒素抑制外源性乙酰胆碱诱发的肌条收缩作用类似阿托品,但机制尚不明,可能A型肉毒毒素作用于突触后膜受体或者平滑肌上的SNAP-25蛋白,而抑制肌条的收缩。

Inhibitory effect of botulinum toxin type A on acetylcholine induced contractile response in rat pyloric smooth muscle in vitro

AIM：To investigate the effect of botulinum toxin type A（BTX-A） on endogenous and exogenous acetylcholine（ACh） induced contractile response in rat pyloric smooth muscle in vitro. METHODS：The effects of BTX-A and atropine on pyloric contractility-induced respectively by electrical field stimulation（EFS）,which is used to promote endogenous ACh release,and by ACh addition were comparatively evaluated.RESULTS：BTX-A inhibited the pyloric smooth muscle contractility-induced by EFS（P0.001）.Both of atropine and BTX-A significantly abolished pyloric contractility-induced by ACh（P0.001）,but BTX-A incompletely did it.CONCLUSION：The evidence of the inhibitory effect of BTX-A on pyloric contractility-induced by EFS suggests that BTX-A inhibits endogenous ACh release through cleaving SNAP-25 protein within presynaptic membrane.The result of the inhibition of BTX-A on ACh induced pyloric contractile response is similar to atropine,suggests that BTX-A probably acts on postsynaptic receptor or pyloric muscle directly.