Effect of Intraischemic Hypothermia on Expression of c-Fos, c-Jun, and HSP72 After Transient Focal Cerebral Ischemia in Rat Brain

Abstract

Male Wistar rats underwent right middle cerebral artery occlusion for 1 h with the intraluminal suture method. During ischemia, animals were assigned to either a normothermic (NT) or a hypothermic (HT) group. In the NT group the animals were left at ambient temperature (21°C), and the brain temperature was elevated to 40°C during ischemia. In the HT group the animals were put into a cold room (1°C), and the brain temperature was decreased to 30°C. In both groups the animals (n = 4) were sacrificed 48h after reperfusion, and %infarct volume were calculated after 2,3,5-triphenyltetrazolium hydrochloride (TTC) staining. In rat striatum there was no significant difference of %infarct volume between the NT and HT groups. In contrast, the %infarct volume of the cortex was decreased in the HT group compared with that in NT group. To evaluate the effect of hypothermia on gene expression after transient focal ischemia, animals (n = 5 per time point) were sacrificed at 3,6, and 24 h after reperfusion. Immunohistochemistry was performed at each time point with c-Fos, c-Jun, and HSP72 antibody. Our results revealed that increased c-Fos immunoreactivity in the cortex was observed at 3 h after reperfusion in the NT group but not in HT group, c-Jun expression was not affected by HT treatment, and HSP72 expression in the cortex was decreased in the HT group compared to that in the NT group. In conclusion, hypothermia suppressed aggravation of cerebral infarction, and c-Fos expression in the periinfarct area of cortex might play a crucial role in cell survival.