基于ICC自噬探讨疏肝健脾法调节功能性消化不良胃肠动力障碍的研究思路

Research Thinking on The Regulation of Gastrointestinal Motility Disorder in FunctionalDyspepsia by Soothing Liver and Strengthening Spleen Based on ICC Autophagy

功能性消化不良(functional dyspepsia,FD)是临床常见的一种功能性胃肠病,其发病率高、病因复杂且病程迁延。Cajal间质细胞(interstitial cells of Cajal,ICC)是胃肠道电活动的起搏细胞,产生和传播慢波,并参与胃肠道神经递质信号的传递。自噬调节是多种疾病潜在的治疗策略,FD中存在ICC自噬,自噬过程可由AMPK-mTOR信号通路调节,且证实与mTOR、AMPK ghrelin的作用具有相关性。疏肝健脾法改善FD胃肠动力效应与ghrelin有关,但疏肝健脾法是否通过AMPK-mTOR信号通路调节ICC自噬,从而介导ghrelin改善FD胃肠动力障碍的作用,目前机制尚不清楚。因此,基于“肝脾相关”理论,以AMPK-mTOR通路介导的ICC自噬为切入点,探讨FD胃肠动力障碍与ICC自噬之间的联系及疏肝健脾法的干预机制,为阐明ghrelin对FD胃肠动力的促进作用与ICC自噬调控的关系提供理论依据。

Functional dyspepsia(FD)is one of the most common functional gastrointestinal diseases in the clinic,with a high incidence,complex etiology,and prolonged course of the disease.Cajal interstitial cells(ICC)are pacemaker cells of gastrointestinal electrical activity,which produce and transmit slow waves and participate in the transmission of gastrointestinal neurotransmitter signals.Autophagy regulation is a potential therapeutic strategy for many diseases.Studies have found that there is ICC autophagy in FD,and AMPK-mTOR signaling pathway regulates the autophagy process,also it has confirmed that mTOR,AMPK and ghrelin are relevant.Additionally,the previous study of our research group has found that ghrelin is mediated the improvement of FD gastrointestinal motility by“Shugan Jianpi Method”.However,it is still unclear whether“Shugan Jianpi Method”can regulate the autophagy of ICC through the AMPK-mTOR signaling pathway,and then mediate the role of ghrelin in improving the gastrointestinal motility disorder of FD.Based on the theory of"liver and spleen correlation"and Used ICC autophagy mediated AMPK-mTOR pathway as the entry point,the present project will investigate the relationship between gastrointestinal motility disorder of FD and ICC autophagy mediated AMPK-mTOR pathway,and study the intervention mechanism of“Shugan Jianpi Method”.The aim is to clarify the relationship of ICC autophagy and the improvement of ghrelin in FD gastrointestinal motility.