Chong Z Z, Feng Y P
Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Zhongguo Yao Li Xue Bao. 1997 Nov;18(6):505-8.
To study the effects of dl-3-n-butylphthalide (NBP) on the changes of thromboxane B2 (TXB2) and 6-keto-PGF1 alpha (6-keto-PGF1 alpha) contents in hippocampus, striatum, and cerebral cortex of rats subjected to focal cerebral ischemia followed by reperfusion.
Focal cerebral ischemia was induced by inserting a nylon suture into intracranial segment of internal carotid artery from external carotid artery and blockade of the origin of middle cerebral artery. For reperfusion, the suture was pulled out to restore the blood flow to the ischemic brain. Determination of TXB2 and 6-keto-PGF1 alpha was performed by RIA method.
Reperfusion following focal cerebral ischemia resulted in increases in TXB2 at 5 min and 6-keto-PGF1 alpha at 30 min and a decrease in the ratio of epoprostenol (PGI2)/thromboxane A2 (TXA2) (6-keto-PGF1 alpha/TXB2) at 5 min in hippocampus, striatum, and cerebral cortex. NBP 10 mg.kg-1 reduced the content of TXB2 without decreasing effect on 6-keto-PGF1 alpha. NBP 20 mg.kg-1 reduced both TXB2 and 6-keto-PGF1 alpha in lesser extent than aspirin (Asp, 20 mg.kg-1). NBP 20 or 10 mg.kg-1 elevated the ratio of PGI2/TXA2 after reperfusion, but Asp 20 mg.kg-1 did not increase the ratio except in striatum at 5 min after reperfusion.
NBP increases the ratio of PGI2/TXA2 which may have beneficial effects on the impaired microcirculation in postischemic brain tissues.
研究丁苯酞(NBP)对大鼠局灶性脑缺血再灌注后海马、纹状体及大脑皮质中血栓素B2(TXB2)和6-酮-前列腺素F1α(6-酮-PGF1α)含量变化的影响。
通过将尼龙线从颈外动脉插入颈内动脉颅内段并阻断大脑中动脉起始部诱导局灶性脑缺血。再灌注时,拔出尼龙线以恢复缺血脑组织的血流。采用放射免疫分析法测定TXB2和6-酮-PGF1α。
局灶性脑缺血再灌注后,海马、纹状体及大脑皮质中TXB2在5分钟时升高,6-酮-PGF1α在30分钟时升高,且5分钟时前列环素(PGI2)/血栓素A2(TXA2)(6-酮-PGF1α/TXB2)比值降低。10mg·kg-1的NBP可降低TXB2含量,而对6-酮-PGF1α无降低作用。20mg·kg-1的NBP降低TXB2和6-酮-PGF1α的程度均小于阿司匹林(Asp,20mg·kg-1)。20mg·kg-1或10mg·kg-1的NBP可使再灌注后PGI2/TXA2比值升高,但20mg·kg-1的Asp除在再灌注后5分钟时纹状体中可升高该比值外,其他部位均未升高。
NBP可升高PGI2/TXA2比值,这可能对缺血后脑组织受损的微循环具有有益作用。