Diabetes inhibits cerebral ischemia-induced astrocyte activation - an observation in the cingulate cortex.

Abstract

The objective of this study was to study the effect of diabetic hyperglycemia on astrocytes after forebrain ischemia. Streptozotocin (STZ)-injected hyperglycemic and vehicle-injected normoglycemic rats were subjected to 15 minutes of forebrain ischemia. The brains were harvested in sham-operated controls and in animals with 1 and 6 h of recirculation following ischemia. Brain damage was accessed by haematoxylin and eosin (H&E) staining, cleaved caspase-3 immunohistochemistry and TdT-mediated-dUTP nick end labeling (TUNEL). Anti-GFAP antibody was employed to study astrocytes. The results showed that the 15-minute ischemia caused neuronal death after 1 and 6 h of reperfusion as revealed by increased numbers of karyopyknotic cells, edema, TUNEL-positive and active caspase-3-positive cells. Ischemia also activated astrocytes in the cingulated cortex as reflected by astrocyte stomata hypertrophy, elongated dendrites and increases in the number of dendrites, and immunoreactivity of GFAP. Diabetic hyperglycemia further enhanced neuronal death and suppressed ischemia-induced astrocyte activation. Further, diabetes-damaged astrocytes have increased withdrawal of the astrocyte end-foot from the cerebral blood vessel wall. It is concluded that diabetes-induced suppression and damages to astrocytes may contribute to its detrimental effects on recovery from cerebral ischemia.

• Authors: Li Jing, Li Mai, Jian-Zhong Zhang, Jian-Gang Wang, Yue Chang, Jian-Da Dong, Feng-Ying Guo, P Andy Li
• Journal: International journal of biological sciences (Int J Biol Sci) Vol. 9 Issue 9 Pg. 980-8 ( 2013) ISSN: 1449-2288 [Electronic] Australia
• PMID: 24163590 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• Glial Fibrillary Acidic Protein
• Caspase 3

Topics

• Animals
• Astrocytes (pathology)
• Brain Ischemia (complications, pathology)
• Caspase 3 (metabolism)
• Diabetes Mellitus, Experimental (complications, pathology)
• Glial Fibrillary Acidic Protein (metabolism)
• Gyrus Cinguli (pathology)
• Hyperglycemia (complications, metabolism, pathology)
• Hypoxia, Brain (metabolism, pathology)
• In Situ Nick-End Labeling
• Male
• Prosencephalon (pathology)
• Rats
• Rats, Sprague-Dawley
• Reperfusion