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作 者:肖树华[1,2] 冯建军[1,2] 郭惠芳[1,2] 焦佩英[1,2] 姚民一[1,2] 焦伟[1,2]
机构地区:[1]中国预防医学科学院寄生虫病研究所 [2]世界卫生组织疟疾,血吸虫病和丝虫病合作中心
出 处:《中国药理学报》1994年第1期69-72,共4页Acta Pharmacologica Sinica
基 金:Project supported by the National Natural Science Founda on of China,№ 39070759.
摘 要:细粒棘球蚴囊壁的延胡索酸酶(FH)活力为911—14333,磷酸烯醇式丙酮酸羧激酶(PEPCK)与丙酮酸激酶(PK)的活力之比为2.2—2.7,表明囊壁的糖代谢以酵解途径为主,感染小鼠用甲苯达唑、阿苯达唑或吡喹酮ig治疗,剂量各为25—50,300和500mg·kg^(-1)·d^(-1),连给7—14d,未见对FH有明显的影响,而PK和PEPCK则可明显被前二种药物所抑制。Echinococcus granulosus cyst wall exhih-ited activities of fumarate hydratase (FH), pyruvate kinase (PK), and phosphoenolpyruvate carboxykinase (PEPCK) with 911-1133, 151-215, and 54-98U, re-spectivity. The ratio of PK/PEPCK was 2. 2- 2. 7, indicating that glycolysis is the main pathway of carbo-l.ydrate metabolism in the cyst wall. When infected mice were treated ig with mebendazole, albendazole or praziquantel at the respective daily dose of 25 - 50, 300. and 500 mg·kg-1 for 7 - 14d, no apparent change of FH activity in the cyst wall was found, while PK and PEPCK activities in the cyst wall were markedly inhibited by mebendazole and albendazoie. The inhibition rates of PK and PEPCK activities in mebendazole group were 85 - 88 % and 90 - 92 %, respectively, while in albendazoie group were 55. 3 and 71. 6% , respectively. The results suggest that PK or PEPCK in the cyst wall may the important site attacked by effective antihydatid drugs.
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