Kashyap A, Saha K, Sehgal V N
Department of Immunology and Microbiology, Vallabhbhai Patel Chest Institute, Delhi, India.
Int J Immunopharmacol. 1992 Nov;14(8):1409-14. doi: 10.1016/0192-0561(92)90012-a.
This paper describes the mechanism of in vitro interaction of human serum complement system with anti-leprosy drugs (dapsone and clofazimine) and anti-lepra reaction drugs such as chloroquine. These drugs could inhibit the complement-mediated lysis of erythrocytes both via direct and alternative pathways, but only at hypertherapeutic doses. Attempts were made to restore the drug depleted complement-mediated lysis of erythrocytes by adding zymosan-treated guinea-pig sera (a source of C142) and also by adding Crat-EDTA sera (a source of C3-C9). Destroyed complement-mediated haemolytic activity by dapsone could be restored by early complement (C142) components, while complement-mediated haemolytic activity blocked by clofazimine could be regenerated by adding both late (C3-C9) and early (C142) complement component. However, chloroquine-mediated inhibition of the complement-mediated haemolysis activity could not be appreciably restored by adding both early and late complement reagents.
本文描述了人血清补体系统与抗麻风病药物(氨苯砜和氯法齐明)以及抗麻风反应药物如氯喹在体外的相互作用机制。这些药物可通过直接途径和替代途径抑制补体介导的红细胞溶解,但仅在超治疗剂量时才会如此。人们尝试通过添加经酵母聚糖处理的豚鼠血清(C142的来源)以及添加Crat - EDTA血清(C3 - C9的来源)来恢复药物消耗的补体介导的红细胞溶解。氨苯砜破坏的补体介导的溶血活性可通过早期补体(C142)成分恢复,而氯法齐明阻断的补体介导的溶血活性可通过添加晚期(C3 - C9)和早期(C142)补体成分来再生。然而,添加早期和晚期补体试剂并不能明显恢复氯喹介导的对补体介导的溶血活性的抑制。