Back N, Steger R
Eur J Pharmacol. 1976 Aug;38(2):313-9. doi: 10.1016/0014-2999(76)90334-4.
The effect of aprotinin, EACA and heparin on the growth of the transplanted rodent Murphy-Sturm lymphosarcoma and on several components of the tumor kinin-forming enzyme system was studied. Therapy was administered for 15 days, 3 times daily, one day after tumor transplant. Tumor weights and biochemical parameters (prekallikrein, kininogen and kininase) were measured on the 8th, 10th, 12th and 15th day of therapy. Both aprotinin and heparin significantly inhibited (p less than 0.01) tumor growth by the 15th day, compared to control, saline-administered animals. EACA did not affect the tumor growth rate at any time period. Tumor prekallikrein and kininogen levels were significantly higher (p less than 0.01) in the aprotinin-treated animals. Kininogen levels were higher in the EACA-treated tumors during the latter phase of growth. None of the agents affected the increase in tumor kininase activity that occured during the growth of the tumors. The tumor inhibition and biochemical data suggest the involvement of proteases in the neoplastic process.
研究了抑肽酶、6-氨基己酸(EACA)和肝素对移植性啮齿动物墨菲-斯特姆淋巴肉瘤生长以及肿瘤激肽形成酶系统若干成分的影响。在肿瘤移植后一天开始治疗,为期15天,每日3次。在治疗的第8、10、12和15天测量肿瘤重量和生化参数(前激肽释放酶、激肽原和激肽酶)。与给予生理盐水的对照动物相比,到第15天时,抑肽酶和肝素均显著抑制(p<0.01)肿瘤生长。EACA在任何时间段均未影响肿瘤生长速率。在接受抑肽酶治疗的动物中,肿瘤前激肽释放酶和激肽原水平显著更高(p<0.01)。在生长后期,EACA治疗的肿瘤中激肽原水平更高。这些药物均未影响肿瘤生长过程中出现的肿瘤激肽酶活性增加。肿瘤抑制和生化数据表明蛋白酶参与了肿瘤形成过程。