摘要
目的:观察大蒜素对脑局灶缺血大鼠血小板活化功能或经药物诱导的血小板活化功能及其结构的影响。方法:①将SD大鼠随机分为（空白组、大蒜素大剂量组和小剂量组）3组,于末次给予试药1.5h后颈总动脉插管取血,加入诱导剂二磷酸腺苷（ADP）或胶原,测定血小板最大聚集率;②采用化学刺激（FeCl3）诱导血栓闭塞法制备大鼠急性大脑中动脉血栓模型,随机分为（假手术组、模型组、大蒜素大剂量组和小剂量组）4组,给药方法同实验①,颈总动脉插管取血后分离血浆,测定血浆血栓烷B2（TXB2）、6-酮-前列腺素F1a（6-keto-PGF1a）含量;③加入ADP孵育激活后,离心得到血小板沉淀块,透射电镜下观察血小板的超微结构。结果:与空白组或模型组相比,大蒜素大剂量组（10mg/kg）、小剂量组（5mg/kg）均可显著抑制药物诱导的血小板聚集（P<0.01）,且大剂量组显著优于小剂量组（P<0.05）;均可明显降低模型大鼠血浆TXB2的含量,降低TXB2/6-keto-PGF1a比值,大剂量组还显著升高血浆中6-keto-PGF1a水平（P<0.05,P<0.01）;可明显抑制血小板活化过程中超微结构的改变,且有一定的量效关系。结论:大蒜素可能通过抑制血小板聚集,抑制血小板活化时大量释放的活性肽TXA2、促进恢复TXA2/PGI2平衡,抑制血小板激活释放过程中超微结构的改变,从而对脑?
Objective:To observe whether garlicin can modulate the function and structure of platelets in the rat with focal cerebral ischemia or the platelets induced by ADP. Methods: ①SD rats were divided into 3 groups (placebo, garlicin of high dose and garlicin of low dose ). After the last administration of drug, samples of artery blood were taken and then the aggregation rates of platelet induced by ADP or collagen were measured. ②The acute cerebral infarction rat model were made by blocking the middle cerebral artery. The rats were divided into 4 groups (sham, placebo,garlicin of high and low dose), the drug administrations were the same as ①. The plasma TXB2 and 6-keto-PGF10 were determined. ③After incubated with ADP, the ultrastructure of platelets was observed by the electron microscope. Results:Compared with placebo, the platelet aggregation of the 2 garlicin groups was inhibited, that of the high dose group was superior to low dose group. In the garlicin groups, TXB2 level and the ratio of TXB2/6-keto-PGF1α were reduced. In the high dose garlicin group, the 6-keto-PGF1α content increased. Garlicin could inhibited the change of ultrastructure of platelets in the activation process, and the relationship of dose-effect was obvious. Conclusion:Garlicin has curative effect on acute cerebral infarction, and the possible mechanism of which is to inhibit the pktelets aggregation and the change of ultrastructure of platelets in the activation process, and to regulate the ratio of TXB2/6-keto-PGF1α.
出处
《中日友好医院学报》
2002年第3期152-156,F002,共6页
Journal of China-Japan Friendship Hospital
