炎症性肠病动物模型的研究进展

炎症性肠病（inflammatory bowel disease．IBD）系指一组病因不明的慢性肠道炎症性疾病。包括溃疡性结肠炎（ulcerative colitis，UC）和克罗恩病（Crohn’Sdisease，CD）。多数学者认为，IBD是由感染、免疫、环境等多种因素作用于遗传易感人群，引起肠道免疫反应过度亢进、肠黏膜损伤所致。其发病率呈逐年增长趋势．目前尚缺乏有效根治方法。动物模型的制备在IBD研究中的作用日益为人们所重视．本文拟对近年来IBD动物模型的研究进展作一综述。     

生物药物治疗炎症性肠病新进展

炎症性肠病（inflammatory bowel disease，IBD）是一类病因尚不十分明确的慢性非特异性肠道炎症性疾病，包括溃疡性结肠炎（UC）和克罗恩病（CD）。该病在欧美的发病率较高。随着生活和工作环境的改变，我国的发病率正在逐年上升。但迄今为止对IBD仍无有效方法治愈该病。目前临床上用于缓解症状和维持治疗的药物主要有氨基水杨酸类制剂、肾上腺糖皮质激紊和免疫抑制剂等，但疗效不尽如人意。90年代后期生物药物的问世，使炎症性肠病的药物治疗进入了一个新时代。     

中国炎症性肠病诊断治疗规范的共识意见

炎症性肠病（IBD）是一种病因尚不十分清楚的慢性非特异性肠道炎症性疾病，包括溃疡性结肠炎（UC）和克罗恩病（CD）。前者是一种慢性非特异性结肠炎症，病变主要累及结肠黏膜和黏膜下层，范围多自远段结肠开始，可逆行向近段发展，甚至累及全结肠及末段回肠，呈连续性分布。后者为一种慢性肉芽肿性炎症，病变可累及胃肠道各部位，而以末段回肠及其邻近结肠为主，呈穿壁性炎症，多为节段性、非对称性分布。该病在西方国家相当常见，欧洲和北美UC的发病率为（10—20）／10万、患病率达（100～200）／10万；CD的发病率为（5～10）／10万、患病率达（50～100）／10万。     

炎症性肠病与免疫研究的进展

炎症性肠病(Inflammatory bowel disease，IBD)是一种原因不明的慢性非特异性肠道炎症性疾病．包括克罗恩病(Crohn’s Disease．CD)和溃疡性结肠炎(Ulcerative Colitis，UC)。IBD发生以欧美国家为最高，亚洲国家相对较低，全球均有逐渐增高的趋势。近年来，随着我国人民生活方式的改变．本病的发病率也在上升。黏膜免疫是IBD研究的热点之一，人们已认识到免疫功能紊乱并非IBD伴随情况，而是其重要致病因素，本文就这方面的研究进展作一综述。     

对我国炎症性肠病诊断治疗规范的共识意见

炎症性肠病（IBD）是一种病因尚不十分清楚的慢性非特异性肠道炎症性疾病，包括溃疡性结肠炎（UC）和克罗恩病（CD）。前者是一种慢性非特异性结肠炎症，病变主要累及结肠黏膜和黏膜下层，范围多自远段结肠开始，可逆行向近段发展，甚至累及全结肠和末段回肠，呈连续性分布；临床主要表现为腹泻、腹痛和黏液脓血便。后者为一种慢性肉芽肿性炎症，病变可累及胃肠道各部位，[第一段]     

炎症性肠病实验研究的动物模型

炎症性肠病(IBD)主要包括溃疡性结肠炎(UC)和克罗恩病(CD),是一种反复发作的慢性非特异性肠道炎症性疾病,其确切的病因和发病机制至今还不清楚,治疗上也缺乏特异有效的药物[1]。因此,为研究其病因和发病机制以及开发新药物,建立理想的、类似于人类IBD的动物模型就显得非常重要。理想的IBD实验动物模型应具有如下特点:(1)肠道炎症的发生、病程、病理及病理生理学改变应与人类IBD相同或相似;(2)实验动物应具有明确的遗传背景;(3)实验动物应具有已知抗原易于诱导免疫反应的免疫学特点;(4)传统IBD治疗药物对其治疗有效;(5)实验动物在没…     

对我国炎症性肠病诊断治疗规范的共识意见(2007年,济南)

炎症性肠病（IBD）是一种病因尚不明确的慢性非特异性肠道炎症性疾病，包括溃疡性结肠炎（UC）和克罗恩病（CD）。前者是一种慢性非特异性结肠炎症，病变主要累及结肠黏膜和黏膜下层，范围多自远段结肠开始，可逆行向近段发展，甚至累及全结肠及末段回肠，呈连续性分布，临床主要表现为腹泻、腹痛和黏液脓血便。后者为一种慢性肉芽肿性炎症，病变可累及胃肠道各部位，以末段回肠及其邻近结肠为主，呈穿壁性炎症，多呈节段性、非对称性分布，临床主要表现为腹痛、腹泻、瘘管、肛门病变等。     

炎症性肠病基因型动物模型的研究进展

炎症性肠病(inflammatory bowel disease,IBD)动物模型研究已有100多年历史,近年来新兴的基因型动物模型致病机制具有极强的针对性,对于研究其病因、发病机制、疾病发展规律,确定诊断和治疗手段以及新药开发均有重要意义.本文就IBD的基因型动物模型的研究及进展作一综述.     

炎症性肠病的并发症与肠外表现分析

炎症性肠病（inflammatory bowel disease，IBD）包括溃疡性结肠炎（ulcerative colitis，UC）和克罗恩病（Crohn＇s disease，CD），是一类病因未完全明确的肠道慢性非特异性炎性疾病。该病临床表现复杂，并发症严重，肠外表现多样，而且统计资料显示其发生率的变异程度较大，给诊治带来较大困难。国内有关IBD并发症和肠外表现的大宗病例报道较少。本文总结武汉地区IBD并发症和肠外表现的特点，有助于提高对该疾病的认识，临床诊断与治疗。     

成人炎症性肠病的治疗

简介 克罗恩病（CD）和溃疡性结肠炎（UC）统称为炎症性肠病（IBD），是胃肠道炎症性疾病，病因尚不清楚，病理生理机制复杂。尽管UC和CD有许多相似的临床表现，包括腹痛、血性腹泻、体重下降和发热，但仍有显著的不同之处．如CD可以酷似急性阑尾炎发作的腹痛为首发症状，而UC则可能仅表现为便秘和直肠出血。因此，对于IBD的挑战和回报的关键在于对各种疾病表现的认知、熟悉和反应。     

炎症性肠病动物模型研究进展

炎症性肠病（IBD）包括溃疡性结肠炎（UC）和克罗恩病（CD）。目前IBD的确切病因和发病机制尚不清楚。相当一部分IBD的研究成果源于动物模型的研究,因此建立合适的动物模型至关重要。本文就几种常用的IBD实验动物模型作一综述。     

Proteomics in Inflammatory Bowel Disease: Approach Using Animal Models

Recently, proteomics studies have provided important information on the role of proteins in health and disease. In the domain of inflammatory bowel disease, proteomics has shed important light on the pathogenesis and pathophysiology of inflammation and has contributed to the discovery of some putative clinical biomarkers of disease activity. By being able to obtain a large number of specimens from multiple sites and control for confounding environmental, genetic, and metabolic factors, proteomics studies using animal models of colitis offered an alternative approach to human studies. Our aim is to review the information and lessons acquired so far from the use of proteomics in animal models of colitis. These studies helped understand the importance of different proteins at different stages of the disease and unraveled the different pathways that are activated or inhibited during the inflammatory process. Expressed proteins related to inflammation, cellular structure, endoplasmic reticulum stress, and energy depletion advanced the knowledge about the reaction of intestinal cells to inflammation and repair. The role of mesenteric lymphocytes, exosomes, and the intestinal mucosal barrier was emphasized in the inflammatory process. In addition, studies in animal models revealed mechanisms of the beneficial effects of some therapeutic interventions and foods or food components on intestinal inflammation by monitoring changes in protein expression and paved the way for some new possible inflammatory pathways to target in the future. Advances in proteomics technology will further clarify the interaction between intestinal microbiota and IBD pathogenesis and investigate the gene-environmental axis of IBD etiology.     

莱姆病实验动物模型研究

用从我国新疆全沟硬蜱分离培养的莱姆病螺旋体(XS3),实验感染了新西兰白兔、大耳白兔、13号鼠、大白鼠、中国地鼠、金黄地鼠和豚鼠等7种动物。在一只新西兰白兔发现慢性游走性红斑,一只金黄地鼠和一只13号鼠产生关节炎。患病动物都有较高滴度的抗体。这些结果证实。(1)我国全沟硬蜱莱姆病螺旋体具有足够致病的能力;(2)经培养传代的螺旋体的毒力是稳定的,可引起实验动物莱姆病;(3)莱姆病的发病机理可能与免疫应答有关。另外,证实血中螺旋体的浓度较低,持续时间较短。     

Epidemiologic Clues to Inflammatory Bowel Disease

In this article, the recent literature exploring the epidemiology of inflammatory bowel disease (IBD) is reviewed. Epidemiologic studies present data on disease burden, but may also provide clues to disease etiology. The emergence of IBD in developing nations warrants a systematic search for environmental changes in those countries to explain the evolution of IBD. The hygiene hypothesis suggests that an alteration in the microbial environment experienced by the host facilitates the evolution of chronic immune-mediated diseases. One complex database study suggested that areas with high species richness of human intestinal helminthes are areas with genetic changes in interleukin gene loci. In other words, over the years, the microbial ecology has affected human genetics, which in turn would have an impact on immune responses. Other factors affect the gut microbiome, and several studies have explored the increase in incidence of IBD in relation to such factors as exogenous infections, use of antibiotics, and diet.     

Urinary 8-Hydroxydeoxyguanosine Excretion as a Non-Invasive Marker of Neutrophil Activation in Animal Models of Inflammatory Bowel Disease

Background: Because free radicals contribute to ulcerative colitis and Crohn's disease, assessing oxidative load in vivo could provide a surrogate marker of inflammation and disease status. Methods: Electrochemical high-performance liquid chromatography was used to study urinary excretion of 8-hydroxydeoxyguanosine (8-OH-dGUA), formed by reaction of hydroxyl radicals with native DNA, in 2,4,6-trinitrobenzene-sulfonic acid (TNBS) and dextran sulfate (DSS) rat models of bowel inflammation. Bowel myeloperoxidase (MPO) and histopathology were also assessed. Results: TNBS enema (75 mg/kg in 50% ethanol) and oral DSS (6% via drinking water) both yielded an inflammatory response reflected by increases in bowel MPO that were significantly correlated with tissue injury. In both models urinary 8-OH-dGUA excretion was significantly correlated with bowel MPO activity and epithelial injury and remained at control levels when neutrophils (PMN) were eliminated, whereas epithelial injury and crypt erosion persisted despite neutropenia. Conclusions: Urinary 8-OH-dGUA excretion directly reflects PMN activation in vivo, thereby providing a non-invasive surrogate marker for inflammation in these models which is more indicative of PMN activation than either MPO activity, which does not distinguish inactive from active MPO, or epithelial status, which is independent of PMN activation in both models.     

The Implications of Oxidative Stress and Antioxidant Therapies in Inflammatory Bowel Disease: Clinical Aspects and Animal Models

Inflammatory bowel disease (IBD), including Crohn''s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disorder characterized by alternating phases of clinical relapse and remission. The etiology of IBD remains largely unknown, although a combination of patient''s immune response, genetics, microbiome, and environment plays an important role in disturbing intestinal homeostasis, leading to development and perpetuation of the inflammatory cascade in IBD. As chronic intestinal inflammation is associated with the formation of reactive oxygen and reactive nitrogen species (ROS and RNS), oxidative and nitrosative stress has been proposed as one of the major contributing factor in the IBD development. Substantial evidence suggests that IBD is associated with an imbalance between increased ROS and decreased antioxidant activity, which may explain, at least in part, many of the clinical pathophysiological features of both CD and UC patients. Hereby, we review the presently known oxidant and antioxidant mechanisms involved in IBD-specific events, the animal models used to determine these specific features, and also the antioxidant therapies proposed in IBD patients.Key Words: Animal models, antioxidants, Crohn''s disease, lipid peroxidation, reactive oxygen species, ulcerative colitis