Prasad R N, Mahajan R C, Ganguly N K
Immunol Cell Biol. 1987 Jun;65 ( Pt 3):211-6. doi: 10.1038/icb.1987.23.
The immunopharmacokinetics of chloroquine were studied in Plasmodium knowlesi-infected and uninfected rhesus monkeys. In control monkeys, chloroquine depressed the percentage of lymphocyte subpopulation and their proliferative response after the third dose of drug administration. The effect was maximum during day 6 to 10 after initiation of treatment. During this period the plasma level of chloroquine was high. The drug was slowly excreted and recovery in immune functions was noticed by the 20th day of treatment. On the other hand, the drug caused an irreversible effect on the proliferative response of normal lymphocytes following in vitro exposure of cells. Interestingly, while the drug depressed the immune functions of normal animals, it reversed the immunosuppression caused by malarial parasites in infected animals. The probable mechanism of action of the drug has been discussed.
在感染和未感染诺氏疟原虫的恒河猴中研究了氯喹的免疫药代动力学。在对照猴中,氯喹在第三次给药后降低了淋巴细胞亚群的百分比及其增殖反应。在开始治疗后的第6至10天,这种作用最为明显。在此期间,氯喹的血浆水平很高。药物排泄缓慢,在治疗的第20天观察到免疫功能恢复。另一方面该药物在体外使细胞暴露后对正常淋巴细胞的增殖反应产生不可逆的影响。有趣的是,虽然该药物抑制了正常动物免疫功能,但它却逆转了感染动物中疟原虫引起的免疫抑制。本文讨论了该药物可能的作用机制。