Objective:To investigate the protective effect and the mechanism of ulinastatin on the brain ischemic-reperfusion injury in rats. Methods:Male Sprague-Dawley adult rats were randomly allocated to control group, surgery alone group, ischemic-reperfusion brain injury group, and ulinastatin group. Rats in surgery alone group received surgery without ischemic-reperfusion. Rats in ischemic-reperfusion brain surgery group received ischemic-reperfusion brain surgery. Rats in ulinastatin group received intravenous injection of ulinastatin(50μg·kg-1) at the time after ischemic-reperfusion brain injury. The concentrations of S100β and NSE in plasma were measured by ELISA at 6, 24, 72 h after operation. Brain IL-1β and TNF-α were measured by ELISA at 72 h after operation. Results:Compared with control group, the expression of S100β and NSE were enhanced in the surgery alone group, ischemic-reperfusion brain injury group and ulinastatin group at 6, 24, 72 h after operation(P<0.01), and brain expression of IL-1β and TNF-α were enhanced at 72 h after operation(P<0.01). Compared with injury alone group, the expression of S100β and NSE were enhanced in ischemic-reperfusion brain surgery group and ulinastatin group at 6, 24, 72 h after operation(P<0.01) and brain expression of IL-1β, TNF-α were enhanced at 72 h after operation(P<0.01). Compared with ischemic-reperfusion brain injury group, the expression of S100β and NSE were diminished at 6, 24, 72 h after operation(P<0.01) and the expression of IL-1β and TNF-α were diminished at 72 h after operation in ulinastatin group(P<0.01). Conclusion:Ulinastatin can restrain inflammation in central nervous system and diminish the nervous impairment after ischemic-reperfusion brain injury in rats. |