Propofol Increases Expression of Basic Fibroblast Growth Factor After Transient Cerebral Ischemia in Rats

Abstract

Anesthetics such as propofol can provide neuroprotective effects against cerebral ischemia. However, the underlying mechanism of this beneficial effect is not clear. Therefore, we subjected male Sprague-Dawley rats to 2h of middle cerebral artery occlusion and investigated how post-ischemic administration of propofol affected neurologic outcome and the expression of basic fibroblast growth factor (bFGF). After 2h of ischemia, just before reperfusion, the animals were randomly assigned to receive either propofol (20mgkg(-1)h(-1)) or vehicle (10% intralipid, 2mlkg(-1)h(-1)) intravenously for 4h. Neurologic scores, infarct volume, and brain water content were measured at different time points after reperfusion. mRNA level of bFGF was measured by real-time PCR, and the protein expression level of bFGF was analyzed by immunohistochemistry and Western blot. At 6, 24, 72h, and 7days of reperfusion, infarct volume was significantly reduced in the propofol-treated group compared to that in the vehicle-treated group (all P<0.05). Propofol post-treatment also attenuated brain water content at 24 and 72h and reduced neurologic deficit score at 72h and 7days of reperfusion (all P<0.05). Additionally, in the peri-infarct area, bFGF mRNA and protein expression were elevated at 6, 24, and 72h of reperfusion compared to that in the vehicle-treated group (all P<0.05). These results show that post-ischemic administration of propofol provides neural protection from cerebral ischemia-reperfusion injury. This protection may be related to an early increase in the expression of bFGF.