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目的:观察丁基苯酞(NBP)对大鼠局灶性脑缺血及重灌后海马,纹状体和皮层中TXB2及6ketoPGF1α含量的影响.方法:尼龙线栓塞法造成大鼠局灶性脑缺血模型.TXB2和6ketoPGF1α用放免法测定.结果:NBP10mg·kg-1治疗对缺血重灌注后脑组织中TXB2的产生具有抑制作用,但对6ketoPGF1α的产生无明显作用.NBP20mg·kg-1治疗后,重灌5min缺血脑组织中TXB2和重灌后30min时6ketoPGF1α含量皆明显减少.NBP20或10mg·kg-1皆明显提高PGI2/TXA2的比值.而阿司匹林(20mg·kg-1)除重灌5min提高纹状体PGI2/TXA2的比值外,在其它时间点上均无提高作用.结论:NBP提高缺血脑组织中PGI2/TXA2的比值,可能有利于改善缺血脑组织的微循环状态.
Objective: To observe the effects of butylphthalide (NBP) on TXB2 and 6ketoPGF1α in hippocampus, striatum and cortex after focal cerebral ischemia and reperfusion in rats. Methods: Nylon thread embolism induced focal cerebral ischemia model in rats. TXB2 and 6 kito PGF1α by radioimmunoassay. Results: NBP10mg · kg-1 treatment could inhibit the production of TXB2 in the brain tissue after ischemia-reperfusion, but had no significant effect on the production of 6-keto-PGF1α. NBP20mg · kg-1 treatment, reperfusion 5min ischemic brain tissue TXB2 and 30min after reperfusion 6 keto-PGF1α levels were significantly reduced. NBP20 or 10mg · kg-1 significantly increased the ratio of PGI2 / TXA2. Aspirin (20mg · kg-1) had no effect on PGI2 / TXA2 except at 5 min after reperfusion. Conclusion: NBP increases the ratio of PGI2 / TXA2 in ischemic brain tissue, which may be helpful to improve the microcirculation state of ischemic brain tissue.