共查询到20条相似文献,搜索用时 15 毫秒
1.
2.
3.
Boaz van Driel Gongxian Liao Xavier Romero Michael S. O'Keeffe Guoxing Wang William A. Faubion Scott B. Berger Erica M. Magelky Monika Manocha Veronica Azcutia Matthew Grisham Francis W. Luscinskas Emiko Mizoguchi Rene de Waal Malefyt Hans–Christian Reinecker Atul K. Bhan Ninghai Wang Cox Terhorst 《Gastroenterology》2012
4.
5.
Haiying Li Lillienne Chan Paulina Bartuzi Shelby D. Melton Axel Weber Shani Ben–Shlomo Chen Varol Megan Raetz Xicheng Mao Petro Starokadomskyy Suzanne van Sommeren Mohamad Mokadem Heike Schneider Reid Weisberg Harm-Jan Westra Tõnu Esko Andres Metspalu Vinod Kumar William A. Faubion Felix Yarovinsky Marten Hofker Cisca Wijmenga Michael Kracht Lude Franke Vincent Aguirre Rinse K. Weersma Nathan Gluck Bart van de Sluis Ezra Burstein 《Gastroenterology》2014
6.
7.
8.
9.
10.
11.
12.
13.
Kristina Scheibe Christina Kersten Anabel Schmied Michael Vieth Tatjana Primbs Birgitta Carlé Ferdinand Knieling Jing Claussen Alexander C. Klimowicz Jie Zheng Patrick Baum Sebastian Meyer Sebastian Schürmann Oliver Friedrich Maximilian J. Waldner Timo Rath Stefan Wirtz George Kollias Clemens Neufert 《Gastroenterology》2019,156(4):1082-1097.e11
14.
Kruschewski M Anderson T Loddenkemper C Buhr HJ 《Digestive diseases and sciences》2006,51(8):1461-1470
The role of microcirculation in the pathogenesis and course of chronic inflammatory bowel disease is still unclear. The aim of this study was the evaluation of the role of microcirculation in colitis activity in the rat TNBS (trinitrobenzenesulfonic acid) colitis model using endothelin-1 and a selective endothelin-1 receptor antagonist (LU-135252). Target parameters were capillary blood flow, functional capillary density, vascular permeability, and leukocyte sticking as well as recording of hematocrit, weight course, diuresis, stool quality, and degree of inflammation using a histological colitis score. The acute phase of TNBS colitis is characterized by an extensive disturbance of microcirculation (a significant decrease in capillary blood flow and capillary density and a significant increase in capillary permeability and leukocyte sticking in the mucosa). There is also a significant increase in hematocrit and a significant decrease in diuresis and weight. An exogenous supply of endothelin-1 does not lead to an aggravation of these disorders because of a possible blockage of the endothelin-1 receptors by endogenous endothelin-1 in this florid inflammatory phase. Applying the selective endothelin-1 receptor A antagonist LU-135252 leads to a significant improvement of all microcirculatory parameters and clinical findings compared to the untreated colitis group. Direct improvement of capillary blood flow in the early phase of colitis leads to reduced colitis activity, which underscores the pathogenetic role of the microcirculation in the progression of colitis. 相似文献
15.
Corticotropin-Releasing Factor Regulates TLR4 Expression in the Colon and Protects Mice From Colitis
Zoi Chaniotou Panagiotis Giannogonas Stamatis Theoharis Thalia Teli Jerome Gay Tor Savidge Yassemi Koutmani James Brugni Efi Kokkotou Charalabos Pothoulakis Katia P. Karalis 《Gastroenterology》2010,139(6):2083-2092
16.
Meng-Yu Wang Zi-Xuan Wang Lei-Jie Huang Rui-Xu Yang Zi-Yuan Zou Wen-Song Ge Tian-Yi Ren Jian-Gao Fan 《临床与转化肝病杂志(英文版)》2022,10(5):847
Background and AimsThe concurrence of nonalcoholic steatohepatitis (NASH) and ulcerative colitis (UC) is increasingly seen in clinical practice, but the underlying mechanisms remain unclear. This study aimed to develop a mouse model of the phenomenon by combining high-fat high-cholesterol diet (HFHCD)-induced NASH and dextran sulfate sodium (DSS)-induced UC, that would support mechanistic studies.MethodsMale C57BL/6 mice were randomly assigned to two groups receiving either a chow diet or HFHCD for 12 weeks of NASH modeling. The mice were the divided into four subgroups for UC modeling: (1) A control group given a chow diet with normal drinking water; (2) A colitis group given chow diet with 2% DSS in drinking water; (3) A steatohepatitis group given HFHCD with normal drinking water; and (4) A steatohepatitis + colitis group given HFHCD with 2% DSS in drinking water.ResultsNASH plus UC had high mortality (58.3%). Neither NASH nor UC alone were fatal. Although DSS-induced colitis did not exacerbate histological liver injury in HFHCD-fed mice, premorbid NASH significantly increased UC-related gut injury compared with UC alone. It was characterized by a significantly shorter colon, more colonic congestion, and a higher histopathological score (p<0.05). Inflammatory (tumor necrosis factor-alpha, interleukin 1 beta, C-C motif chemokine ligand 2, and nuclear factor kappa B) and apoptotic (Bcl2, Bad, Bim, and Bax) signaling pathways were significantly altered in distal colon tissues collected from mice with steatohepatitis + colitis compared with the other experimental groups.ConclusionsPremorbid steatohepatitis significantly aggravated DSS-induced colitis and brought about a lethal phenotype. Potential links between NASH and UC pathogeneses can be investigated using this model. 相似文献
17.
18.
Background: Increasing evidence shows that microRNA-7a-5p (miR-7a-5p) plays an important role in regulating the inflammatory process in inflammatory bowel disease (IBD). How miR-7a-5p contributes to this process is poorly defined. The purpose of this study was to examine whether miR-7a-5p regulates 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced inflammatory responses via the JNK pathway.MethodsColitis was induced in male mice by intracolonic administration of TNBS; mice were divided into 3 groups: normal control (NC), TNBS, and miR-7a-5p antagomir-treated group. Inflammatory responses were estimated by disease activity index (DAI) and histological scores. The relative expressions of miR-7a-5p and tight junction protein, ZO-1, were detected by RT-qPCR. Western blot assays were used to estimate the level of JNK pathway proteins and ZO-1. After miRNA-antagomir injection, the extent of colonic tissue injury and expression levels of ZO-1 and JNK in intestinal tissue were compared.ResultsmiR-7a-5p and p-JNK expression were higher in the intestinal tissue of the TNBS group as compared to NC. Inhibition of the expression of miR-7a-5p resulted in significantly decreased expression of p-JNK but increased expression of ZO-1 and promoted the recovery of intestinal mucosa.ConclusionThis work demonstrates a correlation between the JNK pathway and miR-7a-5p in TNBS-induced experimental colitis in mice, which may provide a new research direction for the treatment of IBD. 相似文献
19.
20.
TinaMarie Lieu Gihan Jayaweera Peishen Zhao Daniel P. Poole Dane Jensen Megan Grace Peter McIntyre Romke Bron Yvette M. Wilson Matteus Krappitz Silke Haerteis Christoph Korbmacher Martin S. Steinhoff Romina Nassini Serena Materazzi Pierangelo Geppetti Carlos U. Corvera Nigel W. Bunnett 《Gastroenterology》2014