Cajal间质细胞与胆道系统

Cajal间质细胞(ICC)是一类分布于胃肠道及少部分胃肠外器官,具有胃肠起搏及信号转导等功能的细胞.已有较多报道证实其与一系列胃肠动力性疾病如假性肠梗阻、先天性巨结肠、糖尿病胃轻瘫等疾病的发生密切相关.近年来还发现,ICC在胆道系统的胆囊、胆囊管、Oddi括约肌等多处存在,并参与Oddi括约肌自主节律性运动的调控等活...     

影响胃肠Cajal间质细胞起搏功能的体液因子及其作用

胃肠道平滑肌具有自发性、节律性蠕动的特性,其静息电位呈缓慢起伏波动,即周期性去极化和复极化,称为慢波.Cajal间质细胞(inter-stitial cell of Cajal,ICC)是胃肠道的起搏细胞,产生慢波并传导电兴奋.ICC的数量、结构或功能异常与许多胃肠疾病特别是运动障碍性疾病密切相关.体液因子包括激素、神经递质和神经肽、细胞因子以及局部化学介质等,许多体液因子对于ICC及其起搏功能有直接或间接作用,影响胃肠运动.     

胃肠道Cajal间质细胞

Cajal间质细胞(interstitial cells of Cajal,ICC)是分布在消化道自主神经末梢与平滑肌细胞之间的一类特殊细胞.现已证实,ICC是胃肠道起搏细胞,具有产生、传播慢波的功能,并能传导肠神经系统至平滑肌的信号.2008年11月6日至9日在瑞士召开了第22届国际神经胃肠病学与胃肠动力学术研讨会,会议就ICC研究进行了广泛交流,本文综合会议报告内容,就胃肠道ICC研究进展作一综合复习.     

Cajal间质细胞研究进展

Cajal间质细胞（interstitial cells of Cajal,ICC）是胃肠道的起搏细胞,其功能主要是参与胃肠基本电节律的调控和神经递质信号的转导。目前认为,ICC的发育分化障碍、结构或分布异常,ICC病理损害,     

糖尿病小鼠十二指肠运动的变化

糖尿病(DM)的病因主要是胰岛素分泌不足或胰岛索抵抗.胃肠动力障碍是DM患者的常见并发症之一,其机制尚不清楚.近年来普遍认为,Cajal间质细胞(ICC)广泛分布于胃肠道系统中,是胃肠道慢波的起搏细胞,在维持胃肠道正常的生理功能中发挥重要作用.     

Cajal间质细胞与肠炎性病变

Cajal间质细胞(interstitial cells of Cajal,ICC)是胃肠道运动的起搏细胞,它们参与起搏电流的传导和介导肠神经元与平滑肌细胞之间的神经信号。研究显示,ICC数目减少或缺乏的小肠和结肠将失去正常蠕动活性。证实ICC的病理学改变与胃肠运动障碍相关。炎症可引起胃肠运动障碍,ICC在其病理生理中的作用开始受到关注。对ICC在疾病状态下的作用进行详尽解释,还需要在生理和药理学方面进行更深入的研究。     

Cajal间质细胞与慢传输型便秘

Cajal间质细胞是胃肠道神经系统(ENS)的一种非神经但又与神经密切相关的特殊间质细胞。近年的研究表明Cajal间质细胞(ICC)可能是肠道慢波的起搏者，并参与了NANC神经肌肉信息传递过程，有潜在的控制胃肠道动力的作用，而且与人类胃肠道运动性疾病以及胃肠道肿瘤的发病机制有关。慢传输型便秘(STC)就是胃肠运动性疾病中的一种，它是以结肠动     

Cajal间质细胞与慢传输型便秘研究的现状与趋势

Cajal间质细胞(ICC)是分布在胃肠道神经细胞与平滑肌之间的一种特殊细胞,具有起搏及协调胃肠道运动的功能。研究发现慢传输型便秘(STC)患者结肠组织中Cajal间质细胞数量减少,形态及其网状结构改变,因此ICC的异常可能是STC的重要发病机制。预防或干预ICC的病变,积极改善ICC的功能,协调肠道运动可能是潜在治疗STC的方向。     

Cajal间质细胞与胃肠道间质瘤

Cajal间质细胞(interstitial cells“Cajal,ICC)是一类特殊的胃肠道间质细胞,负责胃肠起搏和介导神经递质传递功能,多种胃肠动力障碍性疾病的发生都与ICC异常有关[1]。胃肠道间质瘤(gastrointestinal stromal tumor,GIST)是消化道间叶组织源性肿瘤,目前普遍认为起源于ICC或向ICC分化的多潜能干细胞[2]。     

Cajal间质细胞与肠炎性病变

Cajal间质细胞(interstitial cells of Cajal，ICC)是胃肠道运动的起搏细胞，它们参与起搏电流的传导和介导肠神经元与平滑肌细胞之间的神经信号。研究显示，ICC数目减少或缺乏的小肠和结肠将失去正常蠕动活性。证实ICC的病理学改变与胃肠运动障碍相关。炎症可引起胃肠运动障碍，ICC在其病理生理中的作用开始受到关注。对ICC在疾病状态下的作用进行详尽解释，还需要在生理和药理学方面进行更深入的研究。     

Genetic contribution to motility disorders of the upper gastrointestinal tract

Motility disorders of the upper gastrointestinal tract encompass a wide range of different diseases. Esophageal achalasia and functional dyspepsia are representative disorders of impaired motility of the esophagus and stomach, respectively. In spite of their variable prevalence, what both diseases have in common is poor knowledge of their etiology and pathophysiology. There is some evidence showing that there is a genetic predisposition towards these diseases, especially for achalasia. Many authors have investigated the possible genes involved, stressing the autoimmune or the neurological hypothesis, but there is very little data available. Similarly, studies supporting a post-infective etiology, based on an altered immune response in susceptible individuals, need to be validated. Further association studies can help to explain this complex picture and find new therapeutic targets. The aim of this review is to summarize current knowledge of genetics in motility disorders of the upper gastrointestinal tract, addressing how genetics contributes to the development of achalasia and functional dyspepsia respectively.     

Beneficial effects of NSAIDs in the gastrointestinal tract.

Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin exert irritant and toxic effects upon the organs of the gastrointestinal tract. NSAID toxicity in the gastrointestinal tract is related, at least in part, to the inhibition of the cyclo-oxygenase (COX) enzyme, leading to a reduction of 'cytoprotective' prostaglandin synthesis. In this paper, examples in which NSAIDs exert beneficial effects in the gastrointestinal tract are discussed. NSAIDs, particularly aspirin, are showing promise in the chemoprevention of colorectal, and, to a lesser degree, oesophageal cancers. The clinical value of NSAIDs in the treatment of established gastrointestinal tract cancers is also worthy of further study. There is good clinical evidence showing the value of diclofenac for the treatment of biliary colic and aspirin or ibuprofen for the prevention of gallstones. NSAIDs also have therapeutic potential against other inflammatory gastrointestinal diseases in the oesophagus and possibly pancreas and liver. To a lesser degree, there is some evidence that NSAIDs may have a therapeutic potential in certain gastrointestinal motility disorders, such as aspirin in the post-irradiation syndrome. It therefore follows that in these cancerous, inflammatory and motility pathologies, prostaglandins exert deleterious effects. The paradox of prostaglandins being 'cytoprotective' and potentially damaging can be explained by considering the enzymic origin of prostaglandins. COX-1 is expressed physiologically while inducible COX-2 is expressed in pathological situations. The beneficial clinical effects of selective COX-2-inhibiting NSAIDs in the gastrointestinal tract deserve further study. This paper challenges the concept of 'cytoprotection'.     

肠神经系统退行性变的研究进展

肠神经系统(enteric nervous system,ENS)可独立调节胃肠道感觉、分泌和运动功能,ENS退行性变可导致胃肠道功能的异常,引起一系列的临床症状,其与胃肠动力性疾病和功能性胃肠病的发病有关。本文就导致ENS退行性变的原因、肠神经元退行性变引起的功能异常及其与临床症状的关联性、可能的治疗靶点等方面的研究进展作一概述。     

胃肠道肥大细胞与肠神经系统的相互作用

作为胃肠道免疫系统重要成员的肥大细胞与肠神经系统(ENS)间存在复杂的相互作用,其对胃肠道正常功能的维持至关重要,并与一些疾病的发生密切相关。本文综述了肥大细胞与ENS相互作用的解剖学基础和分子生物学机制及其在胃肠道疾病病理生理学机制中的作用,为探讨相关疾病新的治疗靶点提供了线索。     

Cajal间质细胞与胃肠动力关系的研究进展

Cajal间质细胞(interstitial cells of Cajal,ICC)是胃肠慢波的起搏细胞,具有产生慢波、传导慢波电位、调节神经递质等功能,是调节胃肠动力的重要环节。ICC在维持正常胃肠动力方面发挥着重要作用,同时其形态、数量及分布的改变会导致多种胃肠动力障碍性疾病。一些以ICC为靶向治疗胃肠动力性疾病药物的研究也取得一定进展。本文就近年来ICC与胃肠动力关系的研究进展作一概述。     

Homing of the bone marrow-derived interstitial cells of Cajal is decreased in diabetic mouse intestine

Background: Interstitial cells of Cajal (ICCs), which express c‐Kit receptor tyrosine kinase (KIT), play an important role in gastrointestinal motility. Loss of ICCs likely contributes to diabetic gastrointestinal motility disorder, however, the mechanism of attrition remains unknown. Here, we test the hypothesis that the bone marrow‐derived progenitors are an important source of intestinal ICCs and that decreased homing of these progenitors in diabetes contributes to ICC diminution. Methods: Wild type mice were X‐ray irradiated, transplanted with bone marrow (BMT) from green fluorescence protein (GFP)‐transgenic (TG)‐mice and subsequently made diabetic by streptozotocin (STZ) injection. Intestinal homing of GFP‐positive bone marrow‐derived cells was examined 2 or 5 months after STZ treatment. Results: In the BMT‐mice, we found many GFP‐positive bone marrow‐derived cells (BMDCs) in most parts of the intestinal area, the number of BMDCs was significantly decreased in diabetic mice compared with nondiabetic controls. As a representative area, we further examined the myenteric plexus of the proximal small intestine, and found that the cell numbers of ICCs marked by c‐Kit‐positive immunoreactivity were decreased by more than 40% in diabetic versus nondiabetic mice. Furthermore, numbers of c‐Kit+/GFP+ and c‐Kit+/GFP‐ cells were similar in nondiabetic mice, and decreased by 45.8% and 42.0%, respectively, in diabetic mice. Conclusion: These results suggest that the decreased homing from the bone marrow is a major cause of ICC loss in the intestine in diabetes mellitus.     

Identification of TRPM7 channels in human intestinal interstitial cells of Cajal

AIM: To investigate the characteristics of slow electrical waves and the presence of transient receptor potential melastatin-type 7 (TRPM7) in the human gastrointestinal (GI) tract. METHODS: Conventional microelectrode techniques were used to record intracellular electrical responses from human GI smooth muscle tissue. Immunohistochemistry was used to identify TRPM7 channels in interstitial cells of Cajal (ICCs). RESULTS: The human GI tract generated slow electrical waves and had ICCs which functioned as pacemaker cells. Flufenamic acid, a nonselective cation channel blocker, and 2-APB (2-aminoethoxydiphenyl borate) and La3~+, TRPM7 channel blockers, inhibited the slow waves. Also, TRPM7 channels were expressed in ICCs in human tissue. CONCLUSION: These results suggest that the human GI tract generates slow waves and that TRPM7 channels expressed in the ICCs may be involved in the generation of the slow waves.     

Phenotypic alteration of interstitial cells of Cajal in idiopathic sigmoid megacolon

BACKGROUND: Interstitial cells of Cajal (ICCs) are detected as a pacemaker of gastrointestinal movement and express c-kit and CD34. Recently, ICCs have implicated pathogenesis in several human diseases presenting gastrointestinal motor dysfunction. This study was performed to clarify the role of ICCs in idiopathic sigmoid megacolon using histological and immunohistochemical examinations. METHODS: Four adult patients with idiopathic sigmoid megacolon and 11 controls were studied. Histology and immunocytochemistry using NSE, S100, c-kit, and CD34 were performed in conjunction with quantitative analysis using the public domain NIH image program. RESULTS: Little histological change in neuromuscular structures in megacolon was observed. Immunohistochemistry demonstrated remarkable decrease of c-kit expressing ICCs without reduction of CD34 expression in the similar interstitial cell population. This observation was further supported by quantitative assessment using public domain NIH image program. CONCLUSIONS: A specific downregulation of c-kit in ICCs may be a cause of idiopathic sigmoid megacolon in adults.     

Relationship of Helicobacter pylori infection with gastrointestinal motility

The interest of gastroenterologists in the relationship between Helicobacter pylori and gastrointestinal motility emerges from the observation that Helicobacter pylori may be involved in the pathogenesis of functional dyspepsia and that a relatively large percentage of patients with dyspepsia may show impaired gastrointestinal motility. A number of studies have been published on the interaction between Helicobacter pylori infection and gastrointestinal motility with controversial results, and, therefore, there are no definite conclusions, as yet, as to whether Helicobacter pylori is able, at all, or in which degree, to influence the motility of the upper gastrointestinal tract. Motility of the upper gastrointestinal tract has been studied in Helicobacter pylori positive and negative individuals by means of manometry, scintigraphy, radio-opaque markers or by other, recently developed, procedures such as breath tests, ultrasonography, and barostat. The vast majority of studies do not support the hypothesis that Helicobacter pylori may influence gastrointestinal motility. Nearly all these studies are, however, affected by methodological problems related to the small numbers of patients, different methodological approaches, and to the well-known difficulties in studying both gastrointestinal motility and functional dyspepsia.