Hyperglycemia Suppresses c-FosmRNA Expression following Transient Cerebral Ischemia in Gerbils

The c- fos proto-oncogene is activated by transient cerebral ischemia. This activation may signify a specific genetic response to ischemia affecting tolerance to ischemia and ultimate cell survival. Hyperglycemia, which enhances brain injury from transient ischemia, was studied for its effects on this gene system in gerbils by measuring c- fos mRNA 2 h after 20 min of bilateral carotid artery occlusion. Brain c- fos mRNA was increased by ischemia (11.7 ± 5.0, p ≤ 0.05, fold increase) compared to nonischemic controls (1.0 ± 1.3). Pretreatment with 1 g/kg of glucose partially reduced postischemic c- fos mRNA (6.3 ± 1.6, p ≤ 0.05) while 4 g/kg of glucose completely suppressed postischemic c- fos expression (0.7 ± 0.3, p ≤ 0.05). These data indicate that hyperglycemia suppresses normal postischemic gene expression and suggest the possibility that such suppression is a predictor or even a contributor to hyperglycemia-enhanced ischemic brain damage.