Supplementation with 0.1% and 2% vitamin e in diabetic rats: analysis of myenteric neurons immunostained for myosin-V and nNOS in the jejunum

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. HEADINGS -Vitamin E. Diabetes mellitus, experimental. Jejunum. Neurons. Myosin type V. Nitric oxide sinthase. Rats.

Supplementation with L-Glutamine and L-Alanyl-L-Glutamine Changes Biochemical Parameters and Jejunum Morphophysiology in Type 1 Diabetic Wistar Rats

“…[ 48 ] reported that the myenteric plexus regulates mucosal cell proliferation in an inhibitory manner. Loss of myenteric neurons [ 49 ] and enhanced cell body area [ 50 ] of submucous neurons are reported in the literature, and can be associated with reduction of the total number of neurons in diabetes. Tronchini et al .…”

Combination vitamin C and vitamin E prevents enteric diabetic neuropathy in the small intestine in rats

“…Supplementation with these vitamins alone also showed promising results with regard to enteral neuroprotection (Pereira et al 2006;Zanoni et al 2007;Pereira et al 2008;Roldi et al 2009;Zanoni et al 2009). However, other studies that tested the effects of these vitamins alone found that vitamin C ) and vitamin E (Tronchini et al 2012) did not preserve enteric neurons in diabetic rats. These results demonstrate that the combination of these antioxidants may more markedly reduce oxidative stress and thus reduce the deleterious effects of diabetes.…”

Ethyl Acetate Fraction from Trichilia catigua Confers Partial Neuroprotection in Components of the Enteric Innervation of the Jejunum in Diabetic Rats

“…Some studies have shown that both EGCs and enteric neurons are affected by diabetes [11,13,14]. Many studies have sought to verify the action of antioxidants (e.g., quercetin, vitamin E, vitamin C, L-glutamine, and L-glutathione) in diabetic neuropathies [14][15][16][17][18]. The present study evaluated the effects of an ethyl-acetate fraction (EAF) from Trichilia catigua, which has been reported to exert better antioxidant effects than the crude extract [19].…”