J.N. Zanoni

Evaluation of the population of NADPH-diaphorase-stained and myosin-V myenteric neurons in the ileum of chronically streptozotocin-diabetic rats treated with ascorbic acid.

We investigated the effect of the ascorbic acid on the nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d)-stained and myosin-V myenteric neurons in the ileum of chronically diabetic rats. The study was performed 4 months after inducing experimental diabetes with streptozotocin. Diabetic rats showed increased (p<0.05) glycaemia and glycated haemoglobin. Three groups were compared, i.e., nondiabetic rats, diabetic rats and diabetic rats treated with ascorbic acid. Myosin-V immunohistochemistry and NADPH-d histochemistry were employed. We investigated the areas of 500 cell bodies of myosin-V neurons and of 500 NADPH-d-stained neurons from all groups. The quantitative analysis was performed by using an area of 8.96 mm(2) from each ileum. The two groups of diabetic rats and diabetic rats treated with ascorbic acid showed reduction in the number and an increased area of the myosin-V-immunostained myenteric neurons. In addition, we observed increased relative proportion of NADPH-d-stained neurons in diabetic rats and diabetic rats treated with ascorbic acid. However, the area of these neurons in the diabetic rats group was larger than those evidenced in the nondiabetic rats and diabetic rats treated with ascorbic acid.

Effects of Supplementation with Ascorbic Acid for a Period of 120 days on the Myosin-V and NADPHd Positive Myenteric Neurons of the Ileum of Rats

We investigated the effect of ascorbic acid (AA) supplementation on the NADPH‐diaphorase (NADPHd) and myosin‐V myenteric neurons in the ileum of rats, after 4 months of treatment. Two groups were compared, i.e. controls rats (C) and AA‐treated rats (CA). Myosin‐V immunohistochemistry and NADPHd histochemistry were employed. We investigated the areas of 500 cell bodies of myosin‐V neurons and of 500 NADPHd stained neurons from all groups. The quantitative analysis was performed using an area of 8.96 mm2 from each ileum. There was an increase of 21.9% in the myosin‐V immunoreactive myenteric neurons (P > 0.05) and of 22.5% in the NADPHd in group CA when compared with C (P < 0.05). There were no significant differences when we compared the area of myosin‐V stained neurons between groups C and CA. However, we verified an area reduction of 7.5% in NADPHd neurons when comparing group C to group CA (P < 0.05).

Morphoquantitative aspects of nitrergic myoenteric neurons from the stomach of diabetic rats supplemented with acetyl-L-carnitine.

The NADPH‐diaphorase (NADPH‐d) positive myoenteric neurons from the body of the stomach of rats with streptozotocin‐induced diabetes with or without supplementation with acetyl‐L‐carnitine (ALC) were evaluated. At the age of 105 days the animals were divided into four groups: normoglycaemic (C), normoglycaemic supplemented with ALC (CC), diabetic (D) and diabetic supplemented with ALC (DC). The supplementation with ALC (200 mg/kg body weight/day) to groups CC and DC was made during 105 days. After this period the animals were killed and the stomach removed and subjected to the histochemical technique of NADPH‐d for the staining of the neurons of the myoenteric plexus. The area of 500 neurons of each group was investigated, as well as the neuronal density in an area of 23.84 mm2 in each stomach. ALC promoted reduction (P < 0.05) of fasting glycaemia, water ingestion and areas of the profiles of the cell bodies of the NADPH‐d neurons in the diabetic animals. The density of these neurons was not statistically different in the groups studied. It is suggested, therefore, a moderate neuroprotective effect of ALC, because the diminishment of the areas of the neuronal profiles in the supplemented diabetic animals, although being statistically significant relative to the non‐supplemented diabetics, was not sufficient to equal the values from the non‐diabetic controls.