Effect of the ascorbic acid treatment on the NADHd-positive myenteric neurons of diabetic rats proximal colon

Zanoni, Jacqueline Nelisis; Pereira, Renata Virginia Fernandes; Freitas, Priscila de

doi:10.1590/s1516-89132007000100004

Cited by 7 publications

(11 citation statements)

References 23 publications

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“…Fläring et al (15) reported that supplementation with glutamine attenuated glutathione depletion in skeletal muscle of humans. Our group has observed that the loss of myenteric neurons as a consequence of diabetic neuropathy is not similar throughout the entire digestive tube, for instance, the colon is one of the most affected segments (5,42) . It is possible that some segments have a better antioxidant protection than others.…”

Section: Discussionmentioning

confidence: 98%

Effects of L-glutamine supplementation on the myenteric neurons from the duodenum and cecum of diabetic rats

Zanoni

Tronchini

Moure

et al. 2011

Arq. Gastroenterol.

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-Context -Peripheral neuropathy is one of the chronic complications of diabetes mellitus and is directly related to gastrointestinal consequences of the disease. Myenteric neurons are affected in some pathological conditions such as diabetic neuropathy.The imbalance between cellular antioxidants and free radicals, leading to an increase in oxidative stress, is considered one of the main factors responsible for neuronal damages in diabetes. Drugs that reduce the oxidative stress may play a significant role in the treatment of neurological complications of diabetes mellitus. Objective -To evaluate the effect of L-glutamine supplementation on the myenteric neurons from the cecum and duodenum of Wistar rats with streptozotocin-induced diabetes mellitus. Methods -The animals were divided in four groups (n = 5): non-treated normoglycemics, normoglycemics treated with L-glutamine, non-treated diabetics and diabetics treated with L-glutamine from the 4th day of diabetes induction on. The amino acid L-glutamine was added to their diet at 1%. Giemsa's technique was employed to stain the myenteric neurons. We determined the cell body area of 500 neurons in each group studied. The quantitative analysis was performed by sampling in an area of 16.6 mm 2 in the cecum and 3.6 mm 2 in the duodenum of each animal. Results -After the supplementation with L-glutamine in the duodenum, we observed a preservation of neuronal density in groups normoglycemic and diabetic (P<0.05). We also observed a preservation of the cell bodies area in diabetic animals (group treated with L-glutamine) (P<0.05). In the cecum, that preservation was not evident. Conclusion -Supplementation with L-glutamine (1%) promoted a neuroprotective effect on the myenteric neurons from the duodenum of rats, both in terms of natural aging and of diabetes mellitus.

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Section: Discussionmentioning

confidence: 98%

Effects of L-glutamine supplementation on the myenteric neurons from the duodenum and cecum of diabetic rats

Zanoni

Tronchini

Moure

et al. 2011

Arq. Gastroenterol.

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“…Among the chronic complications caused by diabetes, neurological manifestations are the most common, affecting both the autonomic and peripheral nervous systems and impairing the quality of life of patients (Chandrasekharan et al 2011). Our research group found that diabetes mellitus reduced the density of myenteric neurons and enteric neural plasticity in various segments of the digestive system (Takahashi et al 1997;Zanoni et al 1997;Fregonesi et al 2001;Defani et al 2003;Zanoni et al 2003;Pereira et al 2006;Tashima et al 2007;Zanoni et al 2007;De Freitas et al 2008;Roldi et al 2009;Alves et al 2010;Pereira et al 2011;Zanoni et al 2011;Lopes et al 2012;Hermes-Uliana et al 2014). These changes in enteric innervation that arise from diabetes are attributable to persistent hyperglycemia that produces numerous metabolic changes.…”

Section: Introductionmentioning

confidence: 77%

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

Zanoni

Hermes-Uliana

2015

Braz. arch. biol. technol.

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The present study evaluated the effects of supplementation with a combination of vitamin C and vitamin E on NADH-diaphorase-positive (NADH-d + ) and neuronal nitric oxide synthase (nNOS)-immunoreactive myenteric neurons in the duodenum and ileum in diabetic rats. Forty rats were distributed into the following groups: normoglycemic (N), normoglycemic supplemented with vitamin C and vitamin E (NS), diabetic (D), and diabetic supplemented with vitamin C and vitamin E (DS). Vitamin C was added to the drinking water, and vitamin E was incorporated in the diet (1%). After 120 days, the animals were euthanized, and the duodenum and ileum were subjected to NADH-d and nNOS staining. Quantitative and morphometric analyses of myenteric neurons were performed. Diabetes reduced NADH-d + neurons in the D group. The density of nitrergic neurons was not changed by diabetes or vitamin treatment. Hypertrophy of the cell body area of NADH-d + and nNOS-immunoreactive neurons was observed in both intestinal segments. Combined supplementation with vitamin C and vitamin E prevented the reduction of the density of NADH-d+ neurons and hypertrophy, demonstratred by both techniques. Supplementation with a combination of vitamin C and vitamin E promoted myenteric neuroprotection in the small intestine in diabetic rats.

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“…A decrease in the number of myenteric neurons in STZ-induced diabetes in rats was observed in the stomach (Fregonesi et al 2001, Clebis et al 2004, in the duodenum (Romano et al 1996, Buttow et al 1997, Furlan et al 1999, in the ileum (Zanoni et al 2003, Alves et al 2006, in the small intestine as a whole (Hernandes et al 2000), in the cecum (Zanoni et al 2007), in the proximal colon (Furlan et al 2002). We can justify the controversial results for the NADPH-dp neurons in Group D, C, CS and DS when compared to other reports: the diabetes maintenance period as well as the neurochemical phenotype of the stained neurons was not similar.…”

Section: Discussionmentioning

confidence: 99%

“…We can justify the controversial results for the NADPH-dp neurons in Group D, C, CS and DS when compared to other reports: the diabetes maintenance period as well as the neurochemical phenotype of the stained neurons was not similar. Enhanced changes in the neuronal density can be better observed when a generalized neuronal population is stained regardless of their neurochemical phenotype, as occurs, for example, with the use techniques such as the cuprolinic blue (Phillips et al 2004), myosin V (Zanoni et al 2003), NADH-diaphorase (Sant'Ana et al 2001, Young et al 1993, Clebis et al 2004, , Zanoni et al 2007, Silva et al 2008, methylene blue (Hernandes et al 2000), among others, which stain the whole neuronal population, including the nitrergic neurons. When analyzing specific populations, such as NADPH-dp neurons, more specific results were obtained.…”

Section: Discussionmentioning

confidence: 99%

Effects of ascorbic acid supplementation in ileum myenteric neurons of streptozotocin-induced diabetic rats

et al. 2009

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295Pesq. Vet. Bras. 29(4): 295-302, abril 2009 RESUMO.-[Efeitos da suplementação do ácido ascórbico nos neurônios mientéricos do íleo de ratos diabéticos induzidos por estreptozootocina.] A exacerbação do estresse oxidativo e da via do poliol que comprometem o plexo mioentérico são alterações metabóli-cas características do diabetes. O ácido ascórbico (AA) é antioxidante e inibidor da aldose redutase, podendo atuar como neuroprotetor. Verificaram-se os efeitos da suplementação com AA sobre o número e a área do perfil do corpo celular (PC) de neurônios mioentéricos em ratos diabéticos induzidos por estreptozootocina. Formaram-se quatro grupos com cinco animais cada: normoglicêmico (C); diabético (D); diabético tratado com AA (DS); e normoglicêmico tratado com AA (CS). Três vezes por semana administrou-se 50mg de AA para cada animal (grupos DS e CS). Após 90 dias e eutanásia com tiopental, o íleo foi coletado e processado para a técnica da NADPHdiaforase. Não se observaram diferenças (P>0,05) na densidade neuronal entre os grupos. A área do PC foi menor (P<0,05) para os grupos DS e CS, com incidência maior de neurônios com área do PC superior a 200μm 2 para os grupos C e D. Concluiu-se que o AA não influenciou a densidade neuronal do íleo, mas foi neuroprotetor The exacerbation of the oxidative stress and of the polyol pathway which impair damage myenteric plexus are metabolic characteristics of diabetes. The ascorbic acid (AA) is an antioxidant and an aldose reductase inhibitor, which may act as neuroprotector. The effects of AA supplementation on the density and cellular body profile area (CP) of myenteric neurons in STZ-induced diabetes in rats were assessed. Four groups with five animals each were formed: normoglycemic (C); diabetic (D); AA-treated diabetic (DS) and AA-treated normoglycemic (CS). Dosagen of 50mg of AA were given, three times a week, for each animal (group DS and CS). Ninety days later and after euthanasia, the ileum was collected and processed for the NADPH-diaphorase technique. There were no differences (P>0.05) in the neuronal density among the groups. The CP area was lower (P<0.05) in the DS and CS groups, with a higher incidence of neurons with a CP area exceeding 200μm 2 for groups C and D. The AA had no influence on the neuronal density in the ileum but had a neuroprotective effect, preventing the increase in the CP area and allowing a higher number of neurons with a CP area with less than 200μm 2 .INDEX TERMS: Vitamin C, diabetes, intestine, myenteric plexus.

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Effect of the ascorbic acid treatment on the NADHd-positive myenteric neurons of diabetic rats proximal colon

Cited by 7 publications

References 23 publications

Effects of L-glutamine supplementation on the myenteric neurons from the duodenum and cecum of diabetic rats

Effects of L-glutamine supplementation on the myenteric neurons from the duodenum and cecum of diabetic rats

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

Effects of ascorbic acid supplementation in ileum myenteric neurons of streptozotocin-induced diabetic rats

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