抗疟药物ro42 -1611 (arteflene)不影响恶性疟原虫的细胞粘附性和细胞因子诱导特性。

P H Jakobsen, T Staalsø, K Bendtzen, D Stürchler
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引用次数: 0

摘要

本研究的目的是研究抗疟药ro42 -1611体外阻断寄生虫介导的细胞因子诱导的能力,以及体外感染红细胞对黑色素瘤细胞的粘附能力。ro42 -1611在培养物中具有阻断恶性疟原虫生长的生物活性。ro42 -1611对受疟疾抗原或脂多糖刺激的单核细胞释放TNF、il - α或IL-6细胞因子无明显影响,且不影响细胞活力。Ro 42-1611仅轻微抑制受感染红细胞对黑色素瘤细胞的粘附。To 42-1611的治疗作用似乎仅限于其杀死寄生虫的活性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The antimalarial drug, Ro 42-1611 (arteflene), does not affect cytoadherence and cytokine-inducing properties of Plasmodium falciparum malaria parasites.

The purpose of this study was to investigate the ability of the antimalarial drug, Ro 42-1611 to block parasite mediated cytokine induction in vitro as well as cytoadherence of infected erythrocytes to melanoma cells in vitro. The biological activity of Ro 42-1611 was confirmed as it blocked Plasmodium falciparum growth in cultures. Ro 42-1611, had no major effect on TNF, IL-alpha or IL-6 cytokine release from mononuclear cells stimulated with malaria antigens or lipopolysaccharide and it did not affect cell viability. Ro 42-1611 only slightly suppressed cytoadherence of infected erythrocytes to melanoma cells. The therapeutic effect of To 42-1611 appears to be confined to its parasite killing activity.

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