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目的:探讨胃肠舒促胃肠动力的作用机制。方法:组织块法原代培养胃肠平滑肌细胞,实验分胃肠舒低、中、高剂量组、西沙必利组和正常对照组,各组分别用受试药物(正常对照组用DMEM干粉培养基)干扰细胞24 h,采用一氧化氮荧光探针(DAF-FMDA)反应30 min,流式细胞仪检测一氧化氮(NO)释放。结果:胃肠舒大、中剂量组与正常对照组比较,胃肠平滑肌细胞NO释放的荧光强度明显减弱(P<0.01,P<0.05),与西沙必利组相似。结论:胃肠舒促胃肠动力的作用机制可能是通过抑制胃肠平滑肌细胞内NO的生成,进而抑制相关酶的活化,拮抗环磷酸鸟苷(cGMP)的作用,从而使胞内Ca2+增多,Ca2+信号系统引发一系列生理功能而促进胃肠平滑肌收缩效应。
Objective: To investigate the mechanism of gastrointestinal motility and promoting gastrointestinal motility. Methods: The primary culture of gastrointestinal smooth muscle cells was performed by tissue block method. The experiment was divided into low, middle and high dose gastrointestinal group, cisapride group and normal control group. Each group was treated with DMEM (normal control group) The cells were exposed to DAF-FMDA for 24 hours. Nitric oxide (NO) release was detected by flow cytometry. Results: Compared with the normal control group, the fluorescence intensity of NO release in gastrointestinal smooth muscle cells was significantly decreased (P <0.01, P <0.05), similar to cisapride group. Conclusion: The mechanism of gastrointestinal motility and promoting gastrointestinal motility may be through inhibition of NO production in gastrointestinal smooth muscle cells, thereby inhibiting the activation of related enzymes and antagonizing the action of cyclic guanosine monophosphate (cGMP), thereby increasing intracellular Ca2 + Ca2 + signaling system triggers a series of physiological functions to promote gastrointestinal smooth muscle contraction effect.