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基于脑肠交互机制探讨肠道微生物调节IBS-D内脏高敏的研究进展
引用本文:何力,杨力,凌志维,陈敏.基于脑肠交互机制探讨肠道微生物调节IBS-D内脏高敏的研究进展[J].中国实验方剂学杂志,2019,25(11):224-229.
作者姓名:何力  杨力  凌志维  陈敏
作者单位:成都中医药大学, 成都 610075,成都中医药大学, 成都 610075,成都中医药大学, 成都 610075,成都中医药大学 附属医院, 成都 610075
基金项目:国家自然科学基金项目(81774321)
摘    要:腹泻型肠易激综合征(IBS-D)是一种生物心理社会病,也是一种多因素相互作用引起的慢性功能性肠病。IBSD的发病与内脏感觉异常、肠道动力学异常、肠黏膜微炎性反应、遗传、饮食不耐受等多种因素有关,其中内脏高敏是IBS-D主要的病理生理机制之一,是一种不明原因出现的肠道对寒冷、不良情绪等刺激因素高度敏感的病理过程,但内脏高敏发生机制尚未完全阐明。IBS-D的发病与脑肠互动功能紊乱密切相关,IBS-D患者由于病情反复常常伴随焦虑、抑郁等精神症状,而长期慢性精神应激易诱发及加重IBS-D内脏高敏状态。脑源性神经营养因子(BDNF)及其高亲和受体络氨酸激酶B(Trk B)是研究脑肠互动神经环路的热点,BDNF于中枢神经系统和胃肠道上大量表达,能促进神经系统的发育,维持成熟神经细胞的正常功能,还能调节胃肠道动力和内脏敏感性,是引起和导致神经疼痛敏感的重要细胞因子。肠道微生物是脑肠互动的关键纽带,人精神异常与肠道微生物环境改变引发的肠道症状密切关联。反复精神刺激(如抑郁、焦虑等)可导致肠道菌群的改变,另一方面,肠道菌群结构的改变与神经系统的发育和大脑的功能密切相关。本文以肠道微生物为切入点,以脑—肠轴为轴线,基于BDNF/Trk B通路,探讨肠道菌群调节IBS-D内脏高敏机制的相关性研究。

关 键 词:腹泻型肠易激综合征  脑肠轴  肠道微生物  内脏高敏  双向沟通
收稿时间:2018/9/13 0:00:00

Effect of Intestinal Microbiota in Regulating Visceral Hypersensitivity of IBS-D Based on Brain-gut Interacting Mechanism
HE Li,YANG Li,LING Zhi-wei and CHEN Min.Effect of Intestinal Microbiota in Regulating Visceral Hypersensitivity of IBS-D Based on Brain-gut Interacting Mechanism[J].China Journal of Experimental Traditional Medical Formulae,2019,25(11):224-229.
Authors:HE Li  YANG Li  LING Zhi-wei and CHEN Min
Institution:Chengdu University of Traditional Chinese Medicine(TCM), Chengdu 610075, China,Chengdu University of Traditional Chinese Medicine(TCM), Chengdu 610075, China,Chengdu University of Traditional Chinese Medicine(TCM), Chengdu 610075, China and Affiliated Hospital of Chengdu University of TCM, Chengdu 610075, China
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).
Keywords:diarrhea-predominant irritable bowel syndrome  brain-gut axis  intestinal microbiota  visceral hypersensitivity  bidirectional communication
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