Effect of Intestinal Microbiota in Regulating Visceral Hypersensitivity of IBS-D Based on Brain-gut Interacting Mechanism / 中国实验方剂学杂志

ABSTRACT

Diarrhea-predominant irritable bowel syndrome (IBS-D) is not only a biological mental disorder, but also a kind of chronic functional bowel disease induced by many factors. The pathogenesis of IBS-D is related to visceral sensory abnormalities, intestinal dynamics abnormalities, intestinal mucosal micro-inflammatory reactions, heredity, dietary intolerance and other factors. The visceral hypersensitivity is one of the main pathophysiology, and refers to an unknown cause of intestinal hypersensitivity to cold, bad mood and other stimuli. However, its mechanism remains unclear. The pathogenesis of IBS-D is closely related to the disturbance of brain and intestinal interaction. IBS-D patients often suffer from anxiety, depression and other psychiatric symptoms due to repeated illness, but long-term chronic mental stress can induce and aggravate IBS-D visceral hypersensitivity. Brain-derived neurotrophic factor (BDNF) and its high-affinity receptor tyrosine kinase B (TrkB) are hotspots in studies about brain-gut axis. BDNF is a highly expressed cytokine in the central nervous system and gastrointestinal tract, and can promote the development of the nervous system, maintain the normal function of mature nerve cells and regulate the gastrointestinal motility and visceral sensitivity. Intestinal microbiota is the key link of brain-gut interaction. Mental disorders are closely related to intestinal symptoms caused by changes in intestinal microbial environment. Repeated mental stimulation can lead to changes in intestinal flora; on the other hand, changes in intestinal flora structure are closely related to the development of the nervous system and the function of the brain. With intestinal microbiota as the study object, this article mainly discusses the effect of intestinal microbiota in regulating visceral hypersensitivity of IBS-D based on brain-gut axis (BDNF/TrkB signaling pathway).