从肠道菌群-胆汁酸代谢轴失调探讨腹泻型肠易激综合征肝郁脾虚的机制

Mechanism of the liver spleen deficiency syndrome of diarrhea-predominant irritable bowel caused by intestinal flora-bile acid metabolism axis imbalance

内脏高敏和肠黏膜屏障损伤是腹泻型肠易激综合征(IBS-D)的重要病理生理机制,肠道菌群-胆汁酸代谢轴失调与其密切相关。新近发现,肠道菌群-胆汁酸代谢轴失调可经TGR5/5-HT/5-HT3R和TGR5-JNK引起内脏高敏与肠黏膜屏障损伤,进而导致脑-肠互动异常。已知IBS-D肝郁脾虚与脑-肠互动异常相关,结合“肝主疏泄调节胆汁分泌与排泄”理论,在临床与基础研究相互印证下,肠道菌群-胆汁酸代谢轴失调导致脑-肠互动异常可能是IBS-D核心病机肝郁脾虚的重要生物学机制之一,这对指导中医药防治IBS-D有重要的理论与实践意义。

Visceral hypersensitive and intestinal mucosal barrier damage are the important pathophysiology of IBS-D,and the intestinal flora-bile acid metabolism axis imbalance is closely related to them.It is recently found that intestinal flora-bile acid metabolism axis imbalance can cause visceral hypersensitivity and intestinal mucosal barrier damage through TGR5/5-HT/5-HT3R and TGR5-JNK,which can then lead to abnormal brain-intestinal interaction.IBS-D liver spleen deficiency associated with brain interaction abnormalities,combined with the‘liver main drainage regulate bile secretion and excretion’theory,in clinical and basic research,intestinal flora-bile acid metabolism axis imbalance lead to abnormal brain interaction may be IBS-D important biological mechanisms,which to guide the prevention and treatment of IBS-D has important theoretical and practical significance.