海风藤新木脂素类成分对缺血脑区血小板活化因子及花生四烯酸代谢的影响

目的　研究海风藤新木脂素类成分等天然血小板活化因子 (PAF)受体拮抗剂对脑缺血后PAF及花生四烯酸(AA)代谢的作用影响 ,探讨内在关系及机制。方法　应用放免法测定大脑中动脉线栓闭塞再通不同时相大脑中动脉供血区顶叶皮质PAF、血栓素B2 浓度。结果　单纯缺血 90min时 ,PAF含量已显著高于对照组 ,再灌注 3h稍有回降 ,随即持续升高至 12h ;对应血栓素B2 值再灌注 3h增加 ,在 18h达高峰 ,两者分别于再灌注 2 4h和 36h降至对照组水平。海风藤新木脂素复合物、海风藤酮及银杏叶类制剂银杏内酯B均能明显抑制PAF和血栓素B2 的升高。结论　局灶性脑缺血再灌注后 ,PAF与AA协同参与了神经细胞损伤的发生及发展过程。两类天然PAF受体拮抗剂均可抑制脑缺血后PAF的过量生成、纠正AA代谢紊乱

Effects of kadsurenin mixture on platelet-activating factor and arachidonic acid metabolism in focal reversible ischemic brain area

Objective To study the relationship between platelet activating factor(PAF) and arachidonic acid and observe the effects of PAF receptor antagonists kadsurenin mixture,kadsurenone,ginkgolide B on PAF and TXA 2 after focal cerebral ischemia reperfusion in rats.Methods Focal cerebral ischemia was induced by inserting a nylon suture into the right intracranial segment of internal carotid artery from external carotid artery to block the origin of middle cerebral artery. For reperfusion,the suture was pulled out to restore the blood flow to the ischemic brain.Senile Wistar rats were randomly devided into twelve groups:sham operated control group,simple ischemia for 90 min group,3 h,6 h,12 h,18 h,24 h,36 h,48 h reperfusion groups,and kadsurenin mixture,kadsurenone,ginkgolide B treated groups.In sham operated rats,the thread was inserted only 9 millimeter.Radioimmunoassay was applied to evaluate the PAF and TXB 2 (stable metabolite of TXA 2) levels in rat ischemic brain tissue.Results Compared with the sham operated control group,a great increase in the PAF concentrations in simple ischemia and 3 h,6 h,12 h,18 h reperfusion groups were observed.In contrast,the marked increase in the TXB 2 level was present after 3 h of reperfusion.The peak levels of PAF and TXB 2 were observed at 12 h and 18 h reperfusion,retuned to basal values at 24 h and 36 h respectively.However,pretreatment with three PAF receptor antagonists as mentioned above significantly alleviated the increase in PAF and TXB 2 levels at 12 h reperfusion.Conclusions It was considered that increase in TXA 2 might be closely related to PAF,which is involved in the progress of ischemic neuropathological damages.Two natural PAF receptorantagonists can reduce the elevation of PAF and TXA 2 and correct the disorder of arachidonic acid after cerebral ischemic reperfusion.