Zhang J P, Qian D H
Research Laboratory of Natural and Synthetic Drugs, College of Pharmacy, Second Military Medical University, Shanghai, China.
Zhongguo Yao Li Xue Bao. 1993 Nov;14(6):542-5.
The antitumor activities of Phytolacca acinosa polysaccharides I (PAP-I) and its effects on the induction of tumor necrosis factor (TNF) and immunological cytotoxicity of peritoneal macrophages were studied. PAP-I was given ip 5-20 mg.kg-1.d-1 x 7 d to ICR mice as priming agent with subsequent lipopolysaccharides (10 micrograms/mouse) iv for TNF production. TNF activity was measured by crystal violet staining assay using L929 cells. PAP-I showed priming activity for TNF production with hepto-splenic hyperplasia in a dose-dependent manner. The peritoneal macrophages treated with PAP-I 10 and 20 mg.kg-1 showed 67 and 74%, respectively, cytotoxicity (the control 34% cytotoxicity) against Meth A cells at effector:target = 40:1. PAP-I 10 and 20 mg.kg-1 prolonged the survival time of mice bearing ascites Meth A tumor from 21 +/- 4 to 32 +/- 10 and 38 +/- 8 d and inhibited the solid Meth A tumor growth with inhibition rate of 28.5 and 55.7%, respectively. These results suggested that the antitumor activities of PAP-I were based on the activation of macrophages and induction of TNF.
研究了商陆多糖I(PAP-I)的抗肿瘤活性及其对肿瘤坏死因子(TNF)诱导和腹腔巨噬细胞免疫细胞毒性的影响。将PAP-I以5-20mg·kg-1·d-1的剂量腹腔注射给ICR小鼠,连续7天作为启动剂,随后静脉注射脂多糖(10μg/小鼠)以产生TNF。采用L929细胞结晶紫染色法测定TNF活性。PAP-I对TNF的产生具有启动活性,并伴有肝脾增生,呈剂量依赖性。用10和20mg·kg-1的PAP-I处理的腹腔巨噬细胞在效应细胞:靶细胞=40:1时,对Meth A细胞的细胞毒性分别为67%和74%(对照组细胞毒性为34%)。10和20mg·kg-¹的PAP-I将荷腹水Meth A肿瘤小鼠的存活时间从21±4天延长至32±10天和38±8天,并抑制实体Meth A肿瘤生长,抑制率分别为28.5%和55.7%。这些结果表明,PAP-I的抗肿瘤活性基于巨噬细胞的激活和TNF的诱导。