摘要
分离纯化的意大利蜜蜂毒Ｍｅｌｉｔｔｉｎ组分活化家兔血小板聚集作用，实验结果表明，Ｍｅｌｉｔｔｉｎ在终浓度为６５μｇ／ｍＬ，其活化家兔血小板的聚集率为５４．９５±１０．９１；分别加入ＡＤＰ清除剂ＣＰ／ＣＰＫ，花生四烯酸环氧化酶抑制剂阿斯匹林及血栓烷合成酶抑制剂咪唑后，不能抑制其聚集作用，聚集率依次为４７．３６±０．２０，５０．９７±１５．６０及５１．８８±１１．４９。ＴＸＢ２放射免疫测出。
Melittin activates rabbit platelets to aggregate, accompanied by a slight formation of thromboxane B2 (117. 51±57. 55 ug/mL) wnich is far lower than one (1445. 65±113. 50 ug/ mL) produced by arachidonic acid. Under the final concentration of 65 ug/mL for Melittin and without any inhibitors, its rabbit platelet aggregstion ratio is 54. 95±10. 91. Even with inhibitors such as ADP scavenger creatine phosphate / creatine phosphokinase, arachidonic acid cyclase inhibitor (aspirin) and thromboxane synthnase inhibitor (imidazotyl), Melittin's aggregation ratios in turn are 47. 36 ± 0. 20, 50. 97± 15. 60 and 51. 88± 11. 49. This shows that CP/CPK, imidazotyl and aspirin do not inhibit the activation of rabbit platelets by Melittin. Therefore Melittin activates rabbit platelets by the third pathway independent of ADP and arachidonic acid. Verapamil, a blocker of Ca2+ channel of platelet, thoroughly inhibits the activation of rabbit platelets by Melittin, besides, when Milittin activated EDTA plasma and citrate sodium plasma,the former's aggregation ratio is lower than the latter' s, thus Melittin-activating platelet has a close relation with ca2+ flow in platelets. Papervine and thelophylline just partly inhibits the activation of rabbit platelets by Melittin, so maybe phosphodiesterase- regulated cAMP pathway is not neccessary or main pathway for Melittin activating rabbit platelets.
出处
《重庆师范学院学报（自然科学版）》
1996年第1期15-20,共6页
Journal of Chongqing Normal University(Natural Science Edition)
