Tronchini Eleandro Aparecido, Trevizan Aline Rosa, Tashima Cristiano Massao, Pereira Renata Virginia Ferreira, Zanoni Jacqueline Nelisis
Department of Morphological Sciences, Universidade Estadual de Maringá, Maringá, PR, Brazil.
Arq Gastroenterol. 2012 Dec;49(4):284-90. doi: 10.1590/s0004-28032012000400010.
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.
The effects of 0.1% and 2% vitamin E on myosin-V- and nNOS-immunoreactive neurons in the jejunum of diabetic rats were investigated.
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.
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.
Supplementation with 2% vitamin E had a neurotrophic effect only in the area of myosin-V-immunoreactive neurons compared with the diabetic group.
糖尿病是一种以高血糖为特征的疾病，若长期未经治疗任其发展，会引发血管和神经并发症，这些并发症会导致糖尿病患者肠道神经系统发生改变。在胃肠道中，糖尿病会促进运动和感觉变化，以及该系统的反射功能变化，导致胃轻瘫、腹泻、便秘、巨结肠、胃肠运输缓慢、胃潴留和扩张，同时蠕动收缩减少或增加。多项研究表明，氧化应激是影响糖尿病患者肠道神经系统的血管和神经并发症的主要原因。
研究0.1%和2%维生素E对糖尿病大鼠空肠中肌球蛋白V和神经元型一氧化氮合酶免疫反应性神经元的影响。
将30只大鼠分为以下几组：正常血糖组、用0.1%维生素E治疗的正常血糖组、用2%维生素E治疗的正常血糖组、糖尿病组、用0.1%维生素E治疗的糖尿病组和用2%维生素E治疗的糖尿病组。测定神经元密度和神经元细胞体面积。
与正常血糖组相比，糖尿病组（糖尿病组）肌球蛋白V免疫反应性神经元数量显著减少。用0.1%维生素E治疗的糖尿病组和用2%维生素E治疗的糖尿病组的密度均未高于糖尿病组（P>0.05）。糖尿病状态下一氧化氮能密度未发生变化（P>0.05）。与正常血糖组相比，用2%维生素E治疗的正常血糖组和糖尿病组中肌球蛋白V和神经元型一氧化氮合酶免疫反应性神经元的面积显著增加。
与糖尿病组相比，补充2%维生素E仅在肌球蛋白V免疫反应性神经元区域具有神经营养作用。
