Supplementation with 0.1% and 2% vitamin e in diabetic rats: analysis of myenteric neurons immunostained for myosin-V and nNOS in the jejunum / Suplementação com vitamina E 0,1% e 2% em ratos diabéticos: análise de neurônios mioentéricos imunomarcados para miosina-V e nNOS no jejuno

CONTEXT: Diabetes mellitus is a disease characterized by hyperglycemia that, when allowed to progress long-term untreated, develops vascular and neurological complications, which are responsible for the development of alterations in the enteric nervous system in diabetic patients. In the gastrointestinal tract, diabetes mellitus promotes motor and sensory changes, and in the reflex function of this system, causing gastroparesis, diarrhea, constipation, megacolon, slow gastrointestinal transit, gastric stasis and dilation with decreased or increased peristaltic contractions. Several studies have shown that oxidative stress is the main responsible for the vascular and neurological complications affecting the enteric nervous system of diabetics. OBJECTIVE: The effects of 0.1% and 2% vitamin E on myosin-V- and nNOS-immunoreactive neurons in the jejunum of diabetic rats were investigated. METHODS: Thirty rats were divided into the groups: normoglycemic, normoglycemic treated with 0.1% vitamin E, normoglycemic treated with 2% vitamin E, diabetic, diabetic treated with 0.1% vitamin E, and diabetic treated with 2% vitamin E. The neuronal density and areas of neuron cell bodies were determined. RESULTS: Diabetes (diabetic group) significantly reduced the number of myosin-V-immunoreactive neurons compared with the normoglycemic group. The diabetic treated with 0.1% vitamin E and diabetic treated with 2% vitamin E groups did not exhibit a greater density than the D group (P>0.05). Nitrergic density did not change with diabetes (P>0.05). The areas of myosin-V- and nNOS-immunoreactive neurons significantly increased in the normoglycemic treated with 2% vitamin E and diabetic groups compared with the normoglycemic group. CONCLUSION: Supplementation with 2% vitamin E had a neurotrophic effect only in the area of myosin-V-immunoreactive neurons compared with the diabetic group.

CONTEXTO: O diabetes mellitus (DM) é uma doença caracterizada pela hiperglicemia que a longo prazo, quando não tratada, desenvolve complicações vasculares e neurológicas, responsáveis pelo desenvolvimento das alterações no sistema nervoso entérico de pacientes diabéticos. Em nível gastrointestinal o DM provoca modificações motoras, sensoriais e na função reflexa desse sistema, podendo ocasionar gastroparesia, diarreia, constipação, megacólon, lentidão do trânsito gastrointestinal, estase e dilatação gástrica com diminuição ou aumento de contrações peristálticas. Diversos estudos têm evidenciado que o estresse oxidativo é o principal responsável pelas complicações vasculares e neurológicas que atingem o sistema nervoso entérico de diabéticos. OBJETIVO: O efeito da vitamina E 0,1% e 2 sobre a miosina-V e nNOS imunorreativas em neurônios do jejuno de ratos diabéticos foram investigados. MÉTODOS: Trinta ratos foram divididos em grupos: normoglicêmicos (NU), normoglicêmicos tratados com vitamina E 0,1% (NE1), normoglicêmicos tratados com vitamina E 2% (NE2), diabético (UD), diabéticos tratados com vitamina E 0,1% (DE1), e diabéticos tratados com vitamina E 2% (DE2). A densidade neuronal e áreas de corpos celulares de neurônios foram determinadas. RESULTADOS: Diabetes (UD grupo) reduziu significativamente o número de neurônios miosina-V imunorreativos quando comparado com o grupo UN. Os grupos DE1 e DE2 não exibem uma maior densidade do que o grupo D (P>0,05). Densidade nitrérgicos não se alterou com diabetes (P>0,05). As áreas dos neurônios miosina-V e nNOS imunorreativos aumentaram significativamente nos grupos NE2 e UD comparados com o grupo UN. CONCLUSÃO: A suplementação com vitamina E 2% teve um efeito neurotrófico apenas na área da miosina-V imunorreativos neurônios em comparação com o grupo UD.

Effects of protein and vitamin B deficiency on blood parameters and myenteric neurons of the colon of rats

The aims of this work were to evaluate the effects of the deficient ingestion of protein and vitamin B on the biochemical and hematologic parameters and on the NADH- and NADPH-diaphorase positive myenteric neurons. The control animals (n=10) received commercial chow and the experimental rats (n=10) received chow with protein level reduced to 8 percent during 120 days. At the time of killing blood was collected for assessment of the blood and hematologic parameters and the ascending colon for quantitative analysis of the neurons of the myenteric plexus. It was observed that the reduction of the protein level to 8 percent coupled to the reduction of the levels of vitamin B in adult rats neither led to qualitative or quantitative changes on red or white blood cells, nor decreased globulin levels, induced the formation of edema or gave rise to clinical signs typical of protein or vitamin B deficiency. On the other hand, the experimental protocol led to less weight gain, change on the body composition with fat deposition; decrease of the values of serum total protein and albumin; reduction of the area of colon and density of nitrergic and NADH-diaphorase myenteric neurons inferior to the expected

Morphometry and acetylcholinesterase activity of the myenteric plexus of the wild mouse Calomys callosus

The myenteric plexus of the digestive tract of the wild mouse Calomys callosus was examined using a histochemical method that selectively stains nerve cells, and the acetylcholinesterase (AChE) histochemical technique in whole-mount preparations. Neuronal density was 1,500 + 116 neurons/cm2 (mean + SEM) in the esophagus, 8,900 + 1,518 in the stomach, 9,000 + 711 in the jejunum and 13,100 + 2,089 in the colon. The difference in neuronal density between the esophagus and other regions was statistically significant. The neuron profile area ranged from 45 to 1,100 mum2. The difference in nerve cell size between the jejunum and other regions was statistically significant. AChE-positive nerve fibers were distributed within the myenteric plexus which is formed by a primary meshwork of large nerve bundles and a secondary meshwork of finer nerve bundles. Most of the nerve cells displayed AChE activity in the cytoplasm of different reaction intensities. These results are important in order to understand the changes occurring in the myenteric plexus in experimental Chagas' disease.