脾气虚证小肠运动异常的VIP/NO信号转导机制初探

Discussion on VIP/NO Signal Transduction Mechanisms of Abnormal Small Intestine Function of Spleen-Deficiency Syndrome

目的探讨脾气虚小肠运动异常的细胞信号转导机制。方法Wistar健康大鼠30只,随机分为正常组、模型组、四君子汤防治组,每组10只。采用“破气苦降加饥饱失常法”塑造大鼠脾气虚证模型,分别采用放射免疫法、硝酸还原酶法及分光光度法测定各组大鼠十二指肠、空肠、回肠平滑肌中血管活性肠肽(VIP)、一氧化氮(NO)含量与一氧化氮合酶(NOS)活性;同步观察各组大鼠十二指肠、空肠、回肠平滑肌张力变化。结果模型组大鼠十二指肠、空肠、回肠平滑肌中VIP、NO含量与NOS活性明显低于正常组和四君子汤组,四君子汤组和正常组之间无显著差别;模型组大鼠十二指肠、空肠、回肠平滑肌张力较正常组和四君子汤组明显增强,但四君子汤组和正常组之间未见明显改变。结论脾气虚证与小肠平滑肌VIP/NO信号通路之间具有较好的相关性,该信号通路变化可能是脾虚证小肠运动异常以及脾虚证主要病理生理机制之一。

Objective To investigate the cellular signal transduction of abnormal small intestine function of spleen-deficiency syndrome. Method Rat model of spleen-qi deficiency was established by the method of ＂dissipating stagnant qi and lowering the adverse qi with bitter drugs and irregularity of food＂ and NO, VIP contents and NOS activity of rats＇ smooth muscles of duodenum, jejunum.ileo were＂ measured respectively by radio-immunity, Nitrate reductase and Spectrophotography. Results The content of VIP, NO and NOS activity of rats smooth muscles of duodenum, jejunum ileo of model group were significantly lower than that of normal group and SiJunzi group, and there had no significant difference between normal group and SiJunzi group. Conclusion The signal channel of VIP/NO may have extensive relationship with the deficiency of spleen qi syndrome, and the alteration of the signal channel may be one of the main mechanism of pathophysioloy of the abnormal small intestine function and deficiency of spleen qi syndrome.