Choosing an Animal Model for the Study of Functional Dyspepsia

Ye, Yang; Wang, Xuerui; Zheng, Yang; Yang, Jing‐Wen; Yang, Nana; Shi, Guang‐Xia; Liu, Cun-Zhi

doi:10.1155/2018/1531958

Cited by 20 publications

(22 citation statements)

References 112 publications

(145 reference statements)

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“…Since we have reported that CD68‐ and CCR2‐positive cells were migrated in the duodenal mucosa of the patients with postinfectious FD, the LPS‐stimulated Ucn 2‐treated rat model could reflect postinfectious functional gastrointestinal disorders. Although there have been some reports of animal models echoing certain clinical features of FD, including rat models in which CRF induced the disturbance of gastric emptying and postinfectious IBS, there have been no animal models reflecting the clinical features of postinfectious FD. In this study, central administration of Ucn 2 aggravated intestinal mucosa in the LPS‐stimulated rat models through the upregulation of the infiltrations of CD68‐ and CCR2‐positive cells and elevation of MPO activity in jejunum and ileum in this model.…”

Section: Discussionmentioning

confidence: 99%

Acotiamide attenuates central urocortin 2‐induced intestinal inflammatory responses, and urocortin 2 treatment reduces TNF‐α productions in LPS‐stimulated macrophage cell lines

Yanagawa

Futagami

Sakasegawa

et al. 2020

Neurogastroenterology Motil

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Background To determine whether central and in vitro administration of urocortin 2 (Ucn 2) affected intestinal inflammatory responses in LPS‐stimulated rat models and macrophage cell lines and acotiamide modified mucosal inflammation in this model. Methods Rats were divided into four groups. LPS‐stimulated group (n = 4); LPS‐ and urocortin 2‐treated group (n = 4); LPS‐ and acotiamide‐treated group (n = 4); and LPS‐, urocortin 2‐, and acotiamide‐treated group (n = 4). CD68‐, CCR2‐, and corticotropin‐releasing hormone receptor type 2 (CRHR2)‐positive cells were assessed by immunostaining. Myeloperoxidase (MPO) activity was measured. TNF‐α, IL‐6, and IL‐4 levels were measured by ELISA method. Gastric emptying and small intestinal transit time were determined using Evans blue. Key Results Central administration of Ucn 2 significantly aggravated infiltrations of CD68‐ and CCR2‐positive cells in the intestinal mucosa of LPS‐stimulated rat models compared to those in LPS treatment alone. Interestingly, acotiamide treatment significantly reduced the migrations of both CD68‐ and CCR2‐positive cells in the jejunum of central Ucn 2‐treated LPS‐stimulated rat models. Acotiamide significantly reduced the expression levels of IkB‐α phosphorylation in LPS‐ and MCP‐1‐stimulated NR8383 cells. Central administration of Ucn 2 significantly delayed gastric emptying. In contrast, Ucn 2 stimulation significantly reduced TNF‐α and IL‐6 productions in LPS‐stimulated NR8383 cells and astressin B reversed the inhibition of TNF‐α production in stimulated NR8383 cells. Acotiamide (30 μmol/L) significantly reduced TNF‐α and IL‐6 productions in LPS‐ and MCP‐1‐stimulated NR8383 cells. Conclusions and Inferences Central and in vitro treatments of Ucn 2 affected intestinal inflammatory responses, respectively, and acotiamide improved them.

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Section: Discussionmentioning

confidence: 99%

Acotiamide attenuates central urocortin 2‐induced intestinal inflammatory responses, and urocortin 2 treatment reduces TNF‐α productions in LPS‐stimulated macrophage cell lines

Yanagawa

Futagami

Sakasegawa

et al. 2020

Neurogastroenterology Motil

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“…Delayed gastric emptying through sympathetic activation (36,137) Increased active ghrelin concentration (137,139,140) Hypersensitivity (134)(135)(136) Hyperpermeability through re-organization of the cytoskeleton (134) Changes in mucosal morphology and decrease of glial cells in the submucosa plexus Increased immune cells infiltration (MC Eo)…”

Section: Stress-related Models Of Fgidmentioning

confidence: 99%

Animal Models for Functional Gastrointestinal Disorders

Accarie

Vanuytsel

2020

Front. Psychiatry

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Functional gastrointestinal disorders (FGID), such as functional dyspepsia (FD) and irritable bowel syndrome (IBS) are characterized by chronic abdominal symptoms in the absence of an organic, metabolic or systemic cause that readily explains these complaints. Their pathophysiology is still not fully elucidated and animal models have been of great value to improve the understanding of the complex biological mechanisms. Over the last decades, many animal models have been developed to further unravel FGID pathophysiology and test drug efficacy. In the first part of this review, we focus on stress-related models, starting with the different perinatal stress models, including the stress of the dam, followed by a discussion on neonatal stress such as the maternal separation model. We also describe the most commonly used stress models in adult animals which brought valuable insights on the brain-gut axis in stress-related disorders. In the second part, we focus more on models studying peripheral, i.e., gastrointestinal, mechanisms, either induced by an infection or another inflammatory trigger. In this section, we also introduce more recent models developed around food-related metabolic disorders or food hypersensitivity and allergy. Finally, we introduce models mimicking FGID as a secondary effect of medical interventions and spontaneous models sharing characteristics of GI and anxiety-related disorders. The latter are powerful models for brain-gut axis dysfunction and bring new insights about FGID and their comorbidities such as anxiety and depression.

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“…RWIS was first discovered by Takagi, and has been widely used to elucidate the mechanism of SGML and screen for potential therapeutic drugs [19][20][21] . RWIS is a powerful multiple stress model that integrates psychological factors (e.g., fear, anger, anxiety and despair) and physiological factors (e.g., hunger, struggle and cold water).…”

Section: Gmls Induced By Rwismentioning

confidence: 99%