Altered physiology of acid secretion in depression‐prone Flinders rats results in exacerbated NSAID and stress‐induced gastric damage

Padol, Ireneusz T.; Wang, C.; Hunt, Richard H.

doi:10.1111/j.1365-2982.2011.01811.x

Cited by 6 publications

(4 citation statements)

References 67 publications

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“…Damage to ICC networks is a common observation in mice and humans with delayed GE. 5 , 6 , 9 To determine whether diabetic Csf1 op/op mice had disrupted ICC networks even though GE was normal, we immunolabeled tissues for Kit and examined the ICC networks. There was no difference in density of Kit-positive ICC between gastric muscularis propria tissues from nondiabetic Csf1 op/op mice ( Figure 6 B ) and tissues from Csf1 op/op mice that had been diabetic for more than 8 weeks (see Figure 6 D ), as scored by two independent, blinded investigators (see Figure 6 F ; Op/Op nondiabetic 6.06 ± 0.37, Op/Op diabetic 6.98 ± 0.14 density; n = 5, P = NS, one-way ANOVA with Dunnett’s post-test).…”

Section: Resultsmentioning

confidence: 99%

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Diabetic Csf1op/op Mice Lacking Macrophages Are Protected Against the Development of Delayed Gastric Emptying

Cipriani

Gibbons

Verhulst

et al. 2016

Cellular and Molecular Gastroenterology and Hepatology

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Background & AimsDiabetic gastroparesis is associated with changes in interstitial cells of Cajal (ICC), neurons, and smooth muscle cells in both animal models and humans. Macrophages appear to be critical to the development of cellular damage that leads to delayed gastric emptying (GE), but the mechanisms involved are not well understood. Csf1op/op (Op/Op) mice lack biologically active Csf1 (macrophage colony stimulating factor), resulting in the absence of Csf1-dependent tissue macrophages. We used Csf1op/op mice to determine the role of macrophages in the development of delayed GE.MethodsAnimals were injected with streptozotocin to make them diabetic. GE was determined weekly. Immunohistochemistry was used to identify macrophages and ICC networks in the gastric muscular layers. Oxidative stress was measured by serum malondialdehyde (MDA) levels. Quantitative reverse-transcription polymerase chain reaction was used to measure levels of mRNA.ResultsCsf1op/op mice had normal ICC. With onset of diabetes both Csf1op/op and wild-type Csf1+/+ mice developed increased levels of oxidative stress (75.8 ± 9.1 and 41.2 ± 13.6 nmol/mL MDA, respectively). Wild-type Csf1+/+ mice developed delayed GE after the onset of diabetes (4 of 13) whereas no diabetic Csf1op/op mouse developed delayed GE (0 of 15, P = .035). The ICC were disrupted in diabetic wild-type Csf1+/+ mice with delayed GE but remained normal in diabetic Csf1op/op mice.ConclusionsCellular injury and development of delayed GE in diabetes requires the presence of muscle layer macrophages. Targeting macrophages may be an effective therapeutic option to prevent cellular damage and development of delayed GE in diabetes.

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Section: Resultsmentioning

confidence: 99%

“… 8 The development of delayed gastric emptying (GE) is associated with reduced expression of the receptor tyrosine kinase, Kit, a marker for interstitial cells of Cajal, 6 impairment of ICC networks and changes in the electrical slow wave recorded from smooth muscle cells. 5 , 9 …”

mentioning

confidence: 99%

Diabetic Csf1op/op Mice Lacking Macrophages Are Protected Against the Development of Delayed Gastric Emptying

Cipriani

Gibbons

Verhulst

et al. 2016

Cellular and Molecular Gastroenterology and Hepatology

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“…A total of 17 pathways were identified with P < 0.05 (after multiple test adjustment) ( Table 4, and Supplementary Table S5). All of these signaling pathways have been shown to have a role in schizophrenia except the gastric acid secretion and bile secretion pathway that may play a role in autism, depression (Horvath et al, 1999;Padol et al, 2012), and Alzheimer's disease (Simpson et al, 1994;Winkler et al, 2015). The pathways linked with schizophrenia include focal adhesion (Fan et al, 2013), axon guidance (Chen et al, 2011), calcium signaling pathway (Berridge, 2013;Hertzberg et al, 2015;Lidow, 2003), ECM-receptor interaction (Lubbers et al, 2014), vascular smooth muscle contraction (Sakakibara et al, 2012), arrhythmogenic right ventricular cardiomyopathy (Kawasaki et al, 2015), regulation of actin cytoskeleton (Criscuolo and Balledux, 1996;Zhao et al, 2015), long-term potentiation (Frantseva et al, 2008;Hasan et al, 2011;Salavati et al, 2015), MAPK signaling pathway (Funk et al, 2012), ABC transporters (Akamine et al, 2016), neuroactive ligand-receptor interaction (Adkins et al, 2012), GnRH signaling pathway (Brambilla F Fau -Rovere et al, 1976), salivary secretion (Toone Bk Fau -Lader and Lader, 1979), cell adhesion molecules (CAMs) (Webster et al, 1999;Zhang et al, 2015) and dilated cardiomyopathy (Finsterer and Stollberger, 2016;Volkov Vs Fau -Volkov and Volkov, 2013).…”

Section: Snps Annotationmentioning

confidence: 99%

Accumulation of Minor Alleles of Common SNPs in Schizophrenia

Lei

Yuan

et al. 2017

Preprint

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Schizophrenia is a common neuropsychiatric disorder with a lifetime risk of 1%. A number of large scale genome wide association studies have identified numerous individual risk single nucleotide polymorphisms (SNPs) whose precise roles in schizophrenia remain unknown. Accumulation of many of these risk alleles has been found to be a more important risk factor. Consistently, recent studies showed a role for enrichment of minor alleles (MAs) in complex diseases. Here we studied the role of MAs in general in schizophrenia using public datasets. Relative to matched controls, schizophrenia cases showed higher minor allele content (MAC), especially for the sporadic cases. By linkage analysis, we identified 82 419 SNPs that could be used to predict 2.2% schizophrenia cases with 100% certainty. Pathway enrichment analysis of these SNPs identified 17 pathways, 15 of which are known to be linked with Schizophrenia with the remaining 2 associated with other mental disorders. These results suggest a role for a collective effect of MAs in schizophrenia and provide a method to genetically screen for schizophrenia.

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“…Previous studies reported that gastric mucosa damage is attributable to multiple factors including chemical factors (smoking, drinking, and drugs), physical factors (improper diet), inflammation, intestinal bacterium, and phycological stress (Padol et al. 2012 ; Haj Kheder et al. 2018 ; Zhou and Zhang 2019 ; Woolf and Rose 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Protective effect of valerian extract capsule (VEC) on ethanol- and indomethacin-induced gastric mucosa injury and ameliorative effect of VEC on gastrointestinal motility disorder

Feng

Dai

et al. 2022

Pharmaceutical Biology

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Context Valerian extract capsule (VEC) is an effective Chinese patent medicine used for gastrointestinal (GI) diseases. Objective To investigate the detailed pharmacological activity for VEC clinical effects in GI diseases. Materials and methods Sprague-Dawley rats were divided into six groups: control, model, and drug-treated (VEC-L, VEC-M, VEC-H, and teprenone). Rats were orally administered VEC (124, 248, 496 mg/kg) and teprenone (21.43 mg/kg) for 3 consecutive days. After 1 h, the five groups (except the control group) were orally given ethanol (10 mL/kg) for 1 h or indomethacin (80 mg/kg) for 7 h. The spasmolytic activity of VEC (0.01–1 mg/mL) on ACh/BaCl 2 -induced New Zealand rabbit smooth muscle contraction was performed. The C57BL/6 mice carbon propelling test evaluated the effects of VEC (248–992 mg/kg) on intestinal motility in normal and neostigmine/adrenaline-induced mice. Results Compared with the model group, VEC treatment reduced the gastric lesion index and mucosal damage. Further experiments showed that the pathological ameliorative effect of VEC was accompanied by augmentation of the enzymatic antioxidant system and cytoprotective marker (COX-1, p < 0.01; PGI2 p < 0.05;), along with the alleviation of the levels of MPO (ethanol: 15.56 ± 0.82 vs. 12.15 ± 2.60, p < 0.01; indomethacin: 9.65 ± 3.06 vs. 6.36 ± 2.43, p < 0.05), MDA (ethanol: 1.66 ± 0.44 vs. 0.81 ± 0.58, p < 0.01; indomethacin: 1.71 ± 0.87 vs. 1.09 ± 0.43, p < 0.05), and inflammatory mediators. VEC decreased the high tone induced by ACh/BaCl 2 and promoted intestinal transit in normal and neostigmine/adrenaline-induced mice. Discussion and conclusions VEC showed a potential gastroprotective effect, suggesting that VEC is a promising phytomedicine for the treatment of GI diseases.

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Altered physiology of acid secretion in depression‐prone Flinders rats results in exacerbated NSAID and stress‐induced gastric damage

Cited by 6 publications

References 67 publications

Diabetic Csf1op/op Mice Lacking Macrophages Are Protected Against the Development of Delayed Gastric Emptying

Diabetic Csf1op/op Mice Lacking Macrophages Are Protected Against the Development of Delayed Gastric Emptying

Accumulation of Minor Alleles of Common SNPs in Schizophrenia

Protective effect of valerian extract capsule (VEC) on ethanol- and indomethacin-induced gastric mucosa injury and ameliorative effect of VEC on gastrointestinal motility disorder

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