三乙酰莽草酸对大鼠局灶性脑缺血再灌注过程中血浆血管活性物质量和脑髓过氧化物酶活性的抑制作用(英文)

目的探索血浆内血管活性物质和白细胞浸润在大鼠局灶性脑缺血再灌损伤中是否影响力不同及三乙酰莽草酸(TSA)的保护作用。方法线栓法制备大鼠大脑中动脉缺血90 min再灌注3 ~48 h模型。分别于缺血开始和缺血60 min时给予TSA 50~200 mg·kg-1ig。分别用荧光分光光度法和放射免疫法测定血浆5-羟色胺(5-HT)和血栓烷素B2(TXB2)含量,化学法测定脑皮层中髓过氧化物酶(MPO)活性。结果大鼠脑缺血再灌注3 ~24 h时血浆5-HT和TXB2含量及脑MPO活性呈时间依赖性升高,48 h后5-HT, TXB2含量降至假手术组水平,而MPO活性仍明显高于未缺血侧脑皮层。TSA(100和200 mg·kg-1)可显著抑制缺血90 min再灌注24 h时血浆5-HT和TXB2含量及脑MPO活性增高。结论大鼠局灶性脑缺血再灌注过程中血浆中血管活性物质量和脑组织中MPO活性表现出不同的时相变化,并且对脑损伤影响力不同,TSA可有效保护缺血脑组织。

Inhibitory effect of triacetylshikimic acid on plasma contents of vasoactive substances and brain myeloperoxidase activity during focal cerebral ischemia- reperfusion in rats

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.