基于肠道微生态探源《黄帝内经》泄泻五脏论

泄泻是一种常见的消化道疾病,严重影响了患者的生活质量.随着微生态学发展,泄泻与肠道微生态失调的联系已得到广泛认可.中医经典《黄帝内经》中的泄泻相关论述涉及病因病机、临床表现与治疗诸方面,尤其是开创了从五脏论治泄泻之先河.肠道菌群是一个"被遗忘的器官",菌群失调是泄泻发病的重要机制.《黄帝内经》泄泻五脏论体现了中医理论的整体观念,与肠道微生态失调内涵高度一致.结合共同的认知基础,本文系统整理了近5年文献库中与五脏相关肠道菌群研究的文献,从《黄帝内经》论治泄泻总概论、以及泄泻从脾、肾、肝、心、肺五脏论治的微生态机制进行分析阐述.研究发现肠道菌群的动态平衡是五脏功能协调的主要特征表现,五脏功能失调又皆能引起肠道菌群紊乱.肠道菌群研究成果将成为未来探究《黄帝内经》泄泻五脏论理论内涵的一个关键的科学支点.     

姜良铎教授论脾胃湿热证辨治

脾胃为后天之本,二者同居中焦属土,生理相近,病理相连。脾属阴,喜燥恶润,主运化水谷精微;胃属阳,喜润恶燥,主受纳腐熟水谷。脾主升清,胃主降浊,二者相辅相成,相互为用。《黄帝内经》云＂饮入于胃,游溢精气,上输于脾。脾气散精,上归于肺,通调水道,下输膀胱。水精四布,五经并行,合于四时五脏阴阳,揆度以为常＂,李东垣《脾胃论》中说＂百病皆由脾胃衰而生也＂。     

泄泻肝气乘脾证的研究进展

泄泻肝气乘脾证是现代常见病.中医通过辨证论治,临床疗效显著,而西医往往仅进行支持治疗.研究泄泻肝气乘脾证的发生机制,对泄泻的临床诊治具有重要的指导作用.本文从中医对泄泻肝气乘脾证的认识、发病因素、临床相应经典方剂应用及肠道微生态角度进行探讨,为泄泻肝气乘脾证的发生机制研究及防治提供借鉴.     

老年杂病复杂症状的健脾疗法

<正>人身体的保养及疾病的调护,皆当从后天之本脾胃着眼。"保胃气,存津液"的思想,贯穿于仲景辩证论治过程的始终,尤其是针对杂病复杂症状的诊治。而其采用的健脾疗法多燮理阴阳,调畅气机。脾行气于三阴,为五脏之本。脾为气血生化之源,脾胃健运,则气血化生有源,机体阴阳俱荣,体魄康健;脾失健运,则气血化生不足,脏腑失于濡养,易于生病。胃行气于三阳,为六腑之本。《黄帝内经》认为饮食不加节制,就会损伤肠胃,九窍不通,百病丛生。故脾胃之气的盛衰,对于内伤杂病     

高血压诊疗中的一个新方向——脾胃功能调理与肠道菌群紊乱

"内伤脾胃,百病由生",脾为后天之本,脾胃功能失调与诸多疾病的发生有着密切的联系。肠道菌群已被证实与高血压的发病密切相关,且其稳态受脾胃功能失调的影响,以肠道菌群失调为切入点,在传统高血压调治上,更有针对性地调理脾胃功能,或许可得到更好的高血压治疗效果。     

中医学对五脏胀病的病因病机及治疗原则认识初探

中医学文献中对"胀病"的记载最早见于《黄帝内经》,将胀病分为五脏胀、六腑胀及奇恒之腑胀,并提出了总的治疗原则。五脏胀即为心胀、肺胀、肝胀、脾胀、肾胀。本研究主要总结中医学对五脏胀病的病因病机及治疗原则的认识,旨在为临床提供诊疗思路。     

《幼幼集成》泄泻论治阐微

清代名医陈复正,自幼知医,及长学道,于幼科一门尤有发挥,著有《幼幼集成》六卷传世。全书首创“赋禀”、“护胎”,并以醒世之言辟惊风之悖谬,晰指纹之精微,传神火之功验,具有极高的学术价值。本文就卷三《泄泻证治》篇作一浅析。1　审因论证,宜别所泻之色经曰:“夫泄泻之本,无不由于脾胃”。泄泻乃脾胃专病,陈氏一遵经旨,以此为泄泻辨治的总纲,并推崇张景岳之论:脾健胃和,则水谷腐化,而为气血以行荣卫。若饮食失节,寒温不调,以致脾胃受伤,则水反为湿,谷反为滞,精化之气不能输化,乃致合污下降,而泄泻作矣。泄泻原因虽多,未有不原于湿者,故《…     

肝脾理论在中医肝病中的应用思考

<正>五脏相关理论是中医经典理论,其理论渊源甚古,《素问·玉机真脏论》~([1])有云:"五脏相通,移皆有次,五脏有病,则各传其所胜"。即提出脏腑间在生理上相互联系,病理上按照相克次序传变。肝脾相关理论,是中医学五脏相关理论的重要组成部分,指肝脾两大功能系统在生理功能、病理传变等方面均存在着密切关系。中医肝病是指各种外感、内伤等致病因素引发的     

肠肝轴-肝病防治中的重要目标

人体肠道内寄居着一个复杂、多样化的微生物群落,促进与其共生关系的宿主的新陈代谢和消化.肝病与肠道菌群的定性(失调)和定量(过度生长)改变密切相关.外在因素如饮食、酒精等,可促进肠道菌群失调.在动物模型中,菌群失调可引起肠道炎症、肠屏障破坏以及细菌性产物移位,进而加剧肝损伤和炎症.在失调的肠道环境中产生的细菌性产物和宿主因素在肝病发病机制中同样重要.本文就肠-肝轴失调在非酒精性脂肪性肝病、酒精性肝病以及肝硬化进展中的作用的研究进展和恢复肠道稳态在肝病防治中的潜在应用价值进行简要综述.     

护胃养生与抗衰老

人体的生理活动,需要依靠饮食物的营养。而饮食营养与脾胃对饮食水谷的运化功能,对于维持机体生命活动息息相关。“人之所受气者,谷也;谷之所注者,胃也;胃者,水谷气血之海也。”说明胃气之盛衰有无,关系到人体的生命活动及其存亡。《素问·玉机真脏论》曰:“五脏者,皆禀气于胃;胃者,五脏之本也。”可见,延缓机体衰老,防止疾病发生,与胃的保健,有着密切的关系。 但就饮食物的消化、吸收功能来讲,脾与胃是密不可分相辅相成的。脾胃健旺,则气血生化有源,内则营血运行充沛,外则肌肤丰盛,机体健康,抗病力亦强;若脾胃功能衰弱,则导致化源不足,脏腑失养,     

Intestinal microbiota in pathophysiology and management of irritable bowel syndrome

Irritable bowel syndrome (IBS) is a functional bowel disorder without any structural or metabolic abnormalities that sufficiently explain the symptoms, which include abdominal pain and discomfort, and bowel habit changes such as diarrhea and constipation. Its pathogenesis is multifactorial: visceral hypersensitivity, dysmotility, psychosocial factors, genetic or environmental factors, dysregulation of the brain-gut axis, and altered intestinal microbiota have all been proposed as possible causes. The human intestinal microbiota are composed of more than 1000 different bacterial species and 10¹⁴ cells, and are essential for the development, function, and homeostasis of the intestine, and for individual health. The putative mechanisms that explain the role of microbiota in the development of IBS include altered composition or metabolic activity of the microbiota, mucosal immune activation and inflammation, increased intestinal permeability and impaired mucosal barrier function, sensory-motor disturbances provoked by the microbiota, and a disturbed gut-microbiota-brain axis. Therefore, modulation of the intestinal microbiota through dietary changes, and use of antibiotics, probiotics, and anti-inflammatory agents has been suggested as strategies for managing IBS symptoms. This review summarizes and discusses the accumulating evidence that intestinal microbiota play a role in the pathophysiology and management of IBS.     

肝源性腹泻62例诊治分析

目的探讨肝源性腹泻的发病机制、诊断要点及治疗体会。方法将本院2012年6月至2013年11月收治的62例肝源性腹泻患者依据治疗效果分为三级治疗,一级治疗给予酪酸梭菌二联活菌散调节肠道菌群;二级治疗给予蒙脱石散收敛、吸附、止泻和复方苯乙哌啶抑制肠蠕动;三级治疗给予生长抑素降低门静脉压力。观察治疗前的总胆红素、白蛋白、总胆汁酸、凝血酶原时间血小板计数、脾脏厚径、脾脏长径、脾静脉宽度、门静脉宽度、大便常规、大便培养和治疗前、治疗后腹泻的次数及腹泻的时间。计量资料采用Spearman秩相关进行统计分析。结果肝源性腹泻以肝硬化失代偿期最多见,腹泻次数,腹泻时间与Child-Pugh的相关系数rs分别为0.71、0.69,P值均0.05,差异有统计学意义,即Child-Pugh分级越高,腹泻程度越重且越易出现,其临床表现无特异性,治疗上轻、中度腹泻以改善肝功能、调节肠道菌群、收敛、抑制肠蠕动为主,重度腹泻以降低门静脉压力为主。结论肝源性腹泻发病机制是多方面的,诊断上无特异性,治疗上以治疗原发性肝病、调节肠道菌群及降低门静脉压力为主,生长抑素对重度腹泻效果显著。     

从肠内营养探讨补土法在克罗恩病中的应用

克罗恩病(Crohn’s disease,CD)是一种复发率极高、病因和发病机制仍然不明的胃肠道慢性肉芽肿性炎症性疾病,好发于回肠末端和结肠,病变严重者可累及各段消化道,青壮年为主要的患病人群,患者多表现出腹泻、腹痛、腹块、瘘管形成和肠梗阻等症状,部分患者还可能伴有发热、营养不良等肠外症状,尚不能治愈,且并发症多,极大程度影响了患者的生活[1]。     

Gut microbiota contributes to the distinction between two traditional Chinese medicine syndromes of ulcerative colitis

BACKGROUND Ulcerative colitis(UC)is considered to be closely associated with alteration of intestinal microorganisms.According to the traditional Chinese medicine(TCM)theory,UC can be divided into two disease syndromes called Pi-Xu-Shi-Yun(PXSY)and Da-Chang-Shi-Re(DCSR).The relationships among gut microbiota,TCM syndromes,and UC pathogenesis have not been well investigated.AIM To investigate the role of gut microbiota in UC and the distinction of microbiota dysbiosis between PXSY and DCSR syndromes.METHODS From May 2015 to February 2016,UC patients presenting to LongHua Hospital who met the established inclusion and exclusion criteria were enrolled in this retrospective study.Fresh stool specimens of UC patients with PXSY or DCSR were collected.The feces of the control group came from the health examination population of Longhua Hospital.The composition of gut bacterial communities in stool samples was determined by the pyrosequencing of 16S ribosomal RNA.The high-throughput sequencing reads were processed with QIIME,and biological functions were predicted using Phylogenetic Investigation of Communities by Reconstruction of Unobserved States.RESULTS The composition of gut bacterial communities in 93 stool samples(30 healthy controls,32 patients with PXSY syndrome,and 31 patients with DCSR syndrome)was determined by the pyrosequencing of 16S ribosomal RNA.Beta diversity showed that the composition of the microbiota was different among the three groups.At the family level,Porphyromonadaceae,Rikeneliaceae,and Lachnospiraceae significantly decreased while Enterococcus,Streptococcus,and other potential pathogens significantly increased in UC patients compared to healthy subjects.At the genus level,Parabacteroides,Dorea,and Ruminococcus decreased while Faeca-libacterium showed increased abundance in UC compared to healthy controls.Five differential taxa were identified between PXSY and DCSR syndromes.At the genus level,a significantly increased abundance of Streptococcus was observed in DCSR patients,while Lachnoclostridium increased in PXSY patients.The differential functional pathways of the gut microbiome between the PXSY and DCSR groups mainly included lipid metabolism,immunity,and the metabolism of polypeptides.CONCLUSION Our study suggests that the gut microbiota contributes to the distinction between the two TCM syndromes of UC.     

Intestinal microbes direct CX3CR1+ cells to balance intestinal immunity

ABSTRACT

Intestinal damage driven by unrestricted immune responses against the intestinal microbiota can lead to the development of inflammatory diseases including inflammatory bowel disease. How such breakdown in tolerance occurs alongside the mechanisms to reinforce homeostasis with the microbiota are a focus of many studies. Our recent work demonstrates coordinated interactions between intact microbiota and CX₃CR1 expressing intestinal antigen presenting cells (APCs) that limits T helper 1 cell responses and promotes differentiation of regulatory T cells (Treg) against intestinal antigens including pathogens, soluble proteins and the microbiota itself. We find a microbial attachment to intestinal epithelial cells is necessary to support these anti-inflammatory immune functions. In this addendum, we discuss how our findings enhance understanding of microbiota-directed homeostatic functions of the intestinal immune system and implications of modulating this interaction in ameliorating inflammatory disease.     

肠道菌群失调与功能性腹泻

功能性腹泻(functional diarrhea,FD)主要表现为排便频次的增多及粪便性状的改变,且至少75%不伴有腹痛。它是临床上常见的一种功能性肠病,其发病率仅位居肠易激综合征之后,我国的发病率显著低于西方国家,但在亚洲相对较高。FD的病因和发病机制复杂,而肠道菌群失调被认为是其主要致病因素之一,因此,调节肠道菌群失调、恢复肠道微生态平衡是治疗FD的有效途径,且国内外多项研究表明,应用微生态制剂可有效调节肠道菌群失调,并能明显缓解FD的症状。本文着重就FD和肠道菌群失调的关系及应用微生态制剂治疗FD的疗效作一概述。     

Functional biostructure of colonic microbiota (central fermenting area, germinal stock area and separating mucus layer) in healthy subjects and patients with diarrhea treated with Saccharomyces boulardii

The colonic content can be compared to a spatially structured high output bioreactor composed of three functionally different regions: a separating mucus layer, a germinal stock area, and a central fermenting area. The stool mirrors this structure and can be used for diagnosis in health and disease. In a first part, we introduce a novel method based on fluorescence in situ hybridization (FISH) of sections of punched-out stool cylinders, which allows quantitatively monitor microbiota in the mucus, the germinal stock and the central fermenting areas. in a second part, we demonstrate the practical implementation of this method, describing the biostructure of stool microbiota in healthy subjects and patients with chronic idiopathic diarrhea treated with Saccharomyces boulardii. Punched stool cylinders from 20 patients with chronic idiopathic diarrhea and 20 healthy controls were investigated using fluorescence in situ hybridization. Seventy-three bacterial groups were evaluated. Fluctuations in assembly of 11 constitutive bacterial groups were monitored weekly for 3 weeks prior to, 3 weeks during, and 3 weeks after oral Saccharomyces boulardii supplementation. Typical findings in healthy subjects were a 5-60 μm mucus separating layer; homogeneous distribution and fluorescence, high concentrations (>10 × 10(10) bacterial/mL) of the three habitual bacterial groups: Bacteroides, Roseburia and Faecalibacterium prausnitzii; and low concentrations of the occasional bacterial groups. The diarrhea could be described in terms of increased separating effort, purging, decontamination, bacterial substitution. Typical findings in diarrhea were: increased thickness of the protective mucus layer, its incorporation in the stool, absolute reduction in concentrations of the habitual bacterial groups, suppression of bacterial metabolism in the central fermenting area (hybridization silence), stratification of the stool structure by watery ingredients, and substitutive increase in the concentrations of occasional bacterial groups. The microbial and clinical symptoms of diarrhea were reversible with Saccharomyces boulardii therapy. The structure-functional analysis of stool microbiota allows to quantitatively monitor colonic malfunction and its response to therapy. Saccharomyces boulardii significantly improves the stool biostructure in patients with chronic idiopathic diarrhea and has no influence on the stool microbiota in healthy subjects.     

肠道菌群：功能性胃肠病的防治新靶点

功能性胃肠病（FGIDs）是一组无器质性改变但存在消化功能异常的疾病,是消化科门诊中常见疾病之一。在 最新的罗马Ⅳ标准中将功能性肠胃病定义为脑-肠互动异常疾病。肠道菌群在脑-肠互动中发挥重要作用,参与功 能性胃肠病发生的多种病理生理机制。肠道菌群失调主要通过增加肠道渗透及内脏高敏感性、改变肠道动力和激活 免疫反应参与FGIDs症状产生。因此,重塑肠道菌群稳态的策略在治疗FGIDs中显示出一定的前景。     

Interactions between the host innate immune system and microbes in inflammatory bowel disease

The intestinal immune system defends against pathogens and entry of excessive intestinal microbes; simultaneously, a state of immune tolerance to resident intestinal microbes must be maintained. Perturbation of this balance is associated with intestinal inflammation in various mouse models and is thought to predispose humans to inflammatory bowel disease (IBD). The innate immune system senses microbes; dendritic cells, macrophages, and epithelial cells produce an initial, rapid response. The immune system continuously monitors resident microbiota and utilizes constitutive antimicrobial mechanisms to maintain immune homeostasis. associations between IBD and genes that regulate microbial recognition and innate immune pathways, such as nucleotide oligomerization domain 2 (Nod2), genes that control autophagy (eg, ATG16L1, IRGM), and genes in the interleukin-23-T helper cell 17 pathway indicate the important roles of host-microbe interactions in regulating intestinal immune homeostasis. There is increasing evidence that intestinal microbes influence host immune development, immune responses, and susceptibility to human diseases such as IBD, diabetes mellitus, and obesity. Conversely, host factors can affect microbes, which in turn modulate disease susceptibility. We review the cell populations and mechanisms that mediate interactions between host defense and tolerance and how the dysregulation of host-microbe interactions leads to intestinal inflammation and IBD.