Supplementation action with ascorbic acid in the morphology of the muscular layer and reactive acetylcholinesterase neurons of ileum of mdx mice

Rocha, Marcelo Lisboa; Lima, Marília Fabiana De Oliveira; Stabille, Sandra Regina; Zanoni, Jacqueline Nelisis; Gagliardo, Karina Martinez; Souto, Melyna Soares; Souza, Rodrigo de; Silva, Jodonai Barbosa da; Yokomizo, Sônia Regina De Almeida; Liberti, Édson Aparecido; Clebis, Naianne Kelly

doi:10.1016/j.autneu.2017.05.001

Cited by 5 publications

(3 citation statements)

References 43 publications

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“…The exacerbation of swallowing difficulties contributes to the broader dysphagia framework in patients with DMD. One outcome is eating disorders due to structural and neurological disorders related to the complex process of swallowing and the decreased strength of masticatory muscles . DMD also compromises the function of the gastrointestinal tract (GIT), mainly by affecting the smooth muscles of the wall, and it causes serious motility disorders .…”

mentioning

confidence: 99%

Evaluation of the gastrointestinal tract in mdx mice: an experimental model of Duchenne muscular dystrophy

Feder

Ierardi

Covre

et al. 2018

APMIS

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This study describes the functional and morphological alterations in the intestines of mdx mice (n = 4) compared with the intestinal features of C57BL/10 mice (n = 7) at 2 months of age. The whole gut transit time (carmine red) and the upper gut transit time (activated charcoal) were measured, and light microscopy was utilized to view stained sections (H&E and picrosirius red) for histological analysis. No significant difference in mean evacuation time for the whole gut was observed between the two groups, but a significant delay in activated charcoal passage was observed in the mdx mice. Visually, a higher concentration of collagen fibers in the submucosal region was apparent in the mdx mice. The concentration of collagen fibers in the stomach and small intestine suggests a direct relationship with the decrease in motility of the upper gastrointestinal tract in the mdx mice. Further experimental studies should be conducted to develop therapeutic alternatives to collagen inhibition to control these manifestations.

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mentioning

confidence: 99%

Evaluation of the gastrointestinal tract in mdx mice: an experimental model of Duchenne muscular dystrophy

Feder

Ierardi

Covre

et al. 2018

APMIS

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“…The results and discussion concerning the body weight of the animals were previously published by our research group [22].…”

Section: Resultsmentioning

confidence: 99%

Action of Ascorbic Acid Supplementation in The Prevention of Morphological Changes in the Myocardium in Mice with Muscular Dystrophy

Lima¹,

Oliveira²,

Lisboa³

et al. 2018

SM Musculoskelet Disord

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Duchenne Muscular Dystrophy inducing fibrosis, oxidative stress and muscle necrosis. In the heart, DMD can lead to cardiac failure and death.Objective: This study evaluated the expression of cyclooxygenase-2 (COX-2) and ventricular histological aspects of Dystrophic mice, as well as the effects of Ascorbic acid (AA) on these parameters.Materials and methods: 60 mice, 30 C57BL/10and 30 C57BL10-Dmdmdx, were distributed into six groups according to their age and treatment (n=10/group): control groups at 30 and 60 days (C30 and C60); Dystrophic animals at 30 and 60 days (D30 and D60); and controls and Dystrophic animals at 60days supplemented with AA (CS60 and DS60). After the trial period, the animals were euthanized and their hearts were collected. Samples were subjected to Masson's Trichrome, Picrosirius Red under polarized light and COX-2 Immunohistochemistrytechniques. Results:The results showed an increase of collagen fibers in the D30 group andreduction in the area occupied by cardiomyocytes in D60. COX-2 expression washigher in the C30, D30 and D60 groups, indicating a probable cellular remodelingprocess in C30 and increased oxidative stress leading to fibrosis in dystrophic animals. Conclusion:AA supplementation prevented muscle loss in DS60 compared to D60, as well as a decrease of fibrosis and the expression of COX-2 in DS60, proving the protective action of AA in the hearts of these animals.

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“…Based on these findings, we assume that thinner muscular layers could have slowed the intestinal transit in the F2 group. In addition, disorders on the myenteric plexus may also contribute to the damage on GI transit, since it is located between the longitudinal and circular layers of the muscular layer ( 32 ).…”

Section: Discussionmentioning

confidence: 99%

Paternal obesity and its transgenerational effects on gastrointestinal function in male rat offspring

Machado

Gama

Beckmann

et al. 2021

Braz J Med Biol Res

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The interplay between obesity and gastrointestinal (GI) motility is contradictory, and the transgenerational influence on this parameter is unknown. We aimed to evaluate the GI function in a model of paternal obesity and two subsequent generations of their male offspring. Newborn male rats were treated with monosodium glutamate (MSG) and composed the F1 generation, while control rats (CONT) received saline. At 90 days, male F1 were mated with non-obese females to obtain male offspring (F2), which later mated with non-obese females for obtaining male offspring of F3 generation. Lee Index analysis was adopted to set up the obesity groups. Alternating current biosusceptometry (ACB) technique was employed to calculate GI transit parameters: mean gastric emptying time (MGET), mean cecum arrival time (MCAT), mean small intestinal transit time (MSITT), and gastric frequency and amplitude of contractions. Glucose, insulin, and leptin levels and duodenal morphometry were measured. F1 obese rats showed a decrease in the frequency and amplitude of gastric contractions, while obese rats from the F2 generation showed accelerated MGET and delayed MCAT and MSITT. Glucose and leptin levels were increased in F1 and F2 generations. Insulin levels decreased in F1, F2, and F3 generations. Duodenal morphometry was altered in all three generations. Obesity may have paternal transgenerational transmission, and it provoked disturbances in the gastrointestinal function of three generations.

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Supplementation action with ascorbic acid in the morphology of the muscular layer and reactive acetylcholinesterase neurons of ileum of mdx mice

Cited by 5 publications

References 43 publications

Evaluation of the gastrointestinal tract in mdx mice: an experimental model of Duchenne muscular dystrophy

Evaluation of the gastrointestinal tract in mdx mice: an experimental model of Duchenne muscular dystrophy

Action of Ascorbic Acid Supplementation in The Prevention of Morphological Changes in the Myocardium in Mice with Muscular Dystrophy

Paternal obesity and its transgenerational effects on gastrointestinal function in male rat offspring

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