ABSTRACT
AIM To explore whether plasma vasoactive substances and neutrophil infiltration make different contribution in cerebral ischemia-reperfusion injury and protective effect of triacetylshikimic acid(TSA). METHODSThe rat models of ischemia 90 min and reperfusion 3-48 h were prepared with middle cerebral artery occlusion. TSA 50-200 mg·kg-1 were given (ig) immediately and 60 min again after the onset of ische- mia. Serotonin and thromboxane B2 (TXB2) concentrations in plasma were detected by fluorescence spectrophotometry and radioimmunoassay respectively. Myeloperoxidase(MPO) activity in brain tissue was quantified by chemical analysis. RESULTS At 3-24 h after reperfusion, the concentrations of plasmic serotonin, TXB2, and brain MPO activity increased obviously in a time-dependent manner. At 48 h after reperfusion, the concentrations of serotonin and TXB2 decreased to the same level of sham. Nevertheless, brain MPO activity remained more elevated than the contralateral cortex. At 24 h after reperfusion, TSA (100 and 200 mg·kg-1) was shown to possess the ability to inhibit the increased plasmic serotonin, TXB2 concentrations, and brain MPO activity induced by focal cerebral ischemia-reperfusion. CONCLUSION Vasoactive substances in plasma and MPO activity in brain tissue show different time courses during focal cerebral ischemia-reperfusion and make different contribution to brain damage. TSA is effective to protect the ischemic brain tissue from ischemia-reperfusion injury.
ABSTRACT
AIM To study the effect of dl-3-n-butylphthalide (dl-NBP) on arachidonic acid(AA) release and phospholipase A2 (PLA2) mRNA in cerebral cortex of rats subjected to focal cerebral ischemia. METHODS Focal cerebral ischemia was induced by inserting a monofilament nylon suture into the internal carotid artery and blocking the origin of the middle cerebral artery. AA was determined with high performance liquid chromatography (HPLC). The PLA2 mRNA expression was evaluated by Northern blot analysis. RESULTS Six hours of cerebral ischemia induced AA release in the ischemic cerebral cortex. dl-NBP (10 or 20 mg·kg-1) and nimodipine (0.5 mg·kg-1) given intraperitoneally 5 min and 120 min again after the onset of ischemia significantly reduced AA concentration in the cerebral cortex (P<0.01). d-NBP, but not l-NBP, decreased AA release in the brain after middle cerebral artery occlusion. The expression of PLA2 mRNA in cerebral cortex induced by cerebral ischemia was also inhibited by dl-NBP and d-NBP (10 or 20 mg·kg-1, ip). CONCLUSION dl-NBP and d-NBP inhibited AA release and PLA2 mRNA expression in the ischemic brain tissue in vivo.