ABSTRACT
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.
Subject(s)
Animals , Male , Rats , Diabetes Mellitus, Experimental/metabolism , Jejunum/innervation , Myenteric Plexus/chemistry , Myosin Type V/analysis , Nitric Oxide Synthase Type I/analysis , Vitamin E/administration & dosage , Vitamins/administration & dosage , Diabetes Mellitus, Experimental/complications , Diabetes Mellitus, Experimental/pathology , Immunohistochemistry , Jejunum/chemistry , Myosin Type V/drug effects , Neurons/chemistry , Neurons/drug effects , Nitric Oxide Synthase Type I/drug effects , Rats, Wistar , StreptozocinABSTRACT
The effect of the treatment with acetyl-L-carnitine (ALC) on neurons releasing the vasoactive intestinal polypeptide (VIP) of the submucous plexus in the jejunum of diabetic rats was the purpose of our investigation. Diabetes (DM) was induced by injecting streptozotocin endovenously (35mg/kg). After sacrificing the animals, the jejunum was collected and processed for VIP detection. Four groups were used: C (non-diabetic), CC (non-diabetic treated with ALC), D (diabetic), DC (diabetes treated with ALC). We analyzed the immunoreactivity and the cellular profile of 126 cell bodies. The treatment with ALC improved some aspects of DM. However, it promoted a small increase in the area of neurons from group CC, suggesting a possible neurotrophic effect. Neurons from groups D and DC showed a large increase in their cellular profile and immunoreactivity when compared to C and CC, suggesting a larger concentration of this neurotransmitter within the neurons that produce it. This observation constitutes a recurrent finding in diabetic animals, suggesting that ALC doesnot interfere in the pathophysiological mechanisms that unchain a higher production and/or neurotransmitter accumulation and increase the profile of the VIP-ergic neurons
Subject(s)
Animals , Male , Rats , Acetylcarnitine/pharmacology , Diabetes Mellitus, Experimental/metabolism , Jejunum/innervation , Neurons/metabolism , Nootropic Agents/pharmacology , Submucous Plexus/drug effects , Vasoactive Intestinal Peptide/metabolism , Blood Glucose/metabolism , Dietary Supplements , Diabetic Neuropathies/physiopathology , Immunohistochemistry , Jejunum/chemistry , Rats, Wistar , Streptozocin , Vasoactive Intestinal Peptide/analysisABSTRACT
An indirect immunoperoxidase technique was employed to demonstrate fibronectin in cryostat sections of small bowel mucosa. Prior exposure of the sections to a solution of pepsin (4 mg/ml) was not essential to localize antigenicity of fibronectin immunohistologically.