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Glucocorticoid Generates ROS to Induce Oxidative Injury in the Hippocampus, Leading to Impairment of Cognitive Function of Rats.

Sato H, Takahashi T, Sumitani K, Takatsu H, Urano S - J Clin Biochem Nutr (2010)

Bottom Line: These results suggest that high-level corticosterone in the serum induces reactive oxygen species (ROS), leading to oxidative damage in the hippocampus.Furthermore, pyramidal cell apoptosis was observed to accompany the loss of glucocorticoid receptors at the cornus ammonis 1 region of the hippocampus.The present results imply that ROS generated from the glycation reaction of increased glucose levels caused by gluconeogenesis activation through glucocorticoid with proteins in the serum attack the hippocampus to induce neurodegeneration, resulting in cognitive deficits in rats.

View Article: PubMed Central - PubMed

Affiliation: Division of Biological Chemistry, Shibaura Institute of Technology, 3-7-5 Toyosu, Kohtoh-ku, Tokyo 135-8548, Japan.

ABSTRACT
The present study attempted to clarify whether over-secretion of glucocorticoids in the serum caused by increased hypothalamus-pituitary-adrenal activity induces oxidative stress in the rat brain, and how the stress causes the emergence of cognitive deficits. When rats were subcutaneously injected with corticosterone, lipid hydroperoxides and protein carbonyls increased markedly in the hippocampus in association with a decrease in activity of antioxidative enzymes, such as superoxide dismutase, catalase and glutathione peroxidase. These results suggest that high-level corticosterone in the serum induces reactive oxygen species (ROS), leading to oxidative damage in the hippocampus. After administration of corticosterone to rats, glucose and superoxide levels in the serum increased markedly. Furthermore, pyramidal cell apoptosis was observed to accompany the loss of glucocorticoid receptors at the cornus ammonis 1 region of the hippocampus. Rats injected with corticosterone showed marked deficits in memory function. The present results imply that ROS generated from the glycation reaction of increased glucose levels caused by gluconeogenesis activation through glucocorticoid with proteins in the serum attack the hippocampus to induce neurodegeneration, resulting in cognitive deficits in rats.

No MeSH data available.


Related in: MedlinePlus

Increase in serum glucose in rats after corticosterone injection. *p<0.05 vs normal control; means ± SE, n = 9 for each group of rats.
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Figure 3: Increase in serum glucose in rats after corticosterone injection. *p<0.05 vs normal control; means ± SE, n = 9 for each group of rats.

Mentions: As corticoids are known to have anti-inflammatory effects and to induce increases in blood sugar levels, the effects of corticosterone on plasma glucose levels were investigated. When rats were subcutaneously administered corticosterone, they showed marked increases in plasma glucose levels at 14 days after injection (Fig. 3). Based on these results, it is evident that corticosterone induced high glucose levels in the serum through activated gluconeogenesis by corticosterone.


Glucocorticoid Generates ROS to Induce Oxidative Injury in the Hippocampus, Leading to Impairment of Cognitive Function of Rats.

Sato H, Takahashi T, Sumitani K, Takatsu H, Urano S - J Clin Biochem Nutr (2010)

Increase in serum glucose in rats after corticosterone injection. *p<0.05 vs normal control; means ± SE, n = 9 for each group of rats.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2966932&req=5

Figure 3: Increase in serum glucose in rats after corticosterone injection. *p<0.05 vs normal control; means ± SE, n = 9 for each group of rats.
Mentions: As corticoids are known to have anti-inflammatory effects and to induce increases in blood sugar levels, the effects of corticosterone on plasma glucose levels were investigated. When rats were subcutaneously administered corticosterone, they showed marked increases in plasma glucose levels at 14 days after injection (Fig. 3). Based on these results, it is evident that corticosterone induced high glucose levels in the serum through activated gluconeogenesis by corticosterone.

Bottom Line: These results suggest that high-level corticosterone in the serum induces reactive oxygen species (ROS), leading to oxidative damage in the hippocampus.Furthermore, pyramidal cell apoptosis was observed to accompany the loss of glucocorticoid receptors at the cornus ammonis 1 region of the hippocampus.The present results imply that ROS generated from the glycation reaction of increased glucose levels caused by gluconeogenesis activation through glucocorticoid with proteins in the serum attack the hippocampus to induce neurodegeneration, resulting in cognitive deficits in rats.

View Article: PubMed Central - PubMed

Affiliation: Division of Biological Chemistry, Shibaura Institute of Technology, 3-7-5 Toyosu, Kohtoh-ku, Tokyo 135-8548, Japan.

ABSTRACT
The present study attempted to clarify whether over-secretion of glucocorticoids in the serum caused by increased hypothalamus-pituitary-adrenal activity induces oxidative stress in the rat brain, and how the stress causes the emergence of cognitive deficits. When rats were subcutaneously injected with corticosterone, lipid hydroperoxides and protein carbonyls increased markedly in the hippocampus in association with a decrease in activity of antioxidative enzymes, such as superoxide dismutase, catalase and glutathione peroxidase. These results suggest that high-level corticosterone in the serum induces reactive oxygen species (ROS), leading to oxidative damage in the hippocampus. After administration of corticosterone to rats, glucose and superoxide levels in the serum increased markedly. Furthermore, pyramidal cell apoptosis was observed to accompany the loss of glucocorticoid receptors at the cornus ammonis 1 region of the hippocampus. Rats injected with corticosterone showed marked deficits in memory function. The present results imply that ROS generated from the glycation reaction of increased glucose levels caused by gluconeogenesis activation through glucocorticoid with proteins in the serum attack the hippocampus to induce neurodegeneration, resulting in cognitive deficits in rats.

No MeSH data available.


Related in: MedlinePlus