Enhancing effect of cholesterol on the elimination of liposomes from circulation is mediated by complement activation

脂质体 化学 补体系统 体内分布 体内 体外 胆固醇 生物物理学 生物化学 药理学 免疫学 免疫系统 生物 生物技术
作者
Tatsuhiro Ishida,Kouichi Funato,Soichi Kojima,Ritsuko Yoda,Hiroshi Kojima
出处
期刊:International Journal of Pharmaceutics [Elsevier BV]
卷期号:156 (1): 27-37 被引量:14
标识
DOI:10.1016/s0378-5173(97)00174-9
摘要

The effects of cholesterol (Chol) content on the biodistribution of liposomes as well as the interaction of liposomes with plasma proteins, primarily complement (C) components, were examined in this study. The elimination of liposomes from blood circulation was enhanced by increasing the Chol content in liposomes. Furthermore, included Chol augmented the rate of liposome degradation as measured by the urinary excretion of 3H-inulin encapsulated in liposomes. We have also examined the effect of liposomal Chol on organ clearance (CL) and renal CL (CLrel). The values of organ CL and CLrel reflect the affinity of liposomes for the organ and the degree of liposome degradation in the blood, respectively. Hepatic CL and CLrel, but not splenic CL, increased with the rise of Chol content in liposomes. The amount of liposome degradation in vitro, which reflects the extent of C activation, was correlated with degradation observed in vivo (CLrel). However, the amount of plasma proteins bound to the liposomes was inversely proportional to the extent of in vitro liposome degradation. We have investigated the role of C activating factor (CAF) (Funato et al., 1994, Plasma factor triggering alternative complement pathway activation by liposomes, Pharm. Res., 11, 372–376) on Chol-dependent-C activation. Our results showed that binding of CAF to the liposomes is directly proportional to the amount of Chol present in the liposome. Thus, C activation by Chol in liposomes may proceed via a mechanism involving CAF. Taken together, these results suggest that increasing the Chol content of liposomes enhances the binding of CAF to the liposomes, which in turn, mediates Chol dependent-C activation, resulting in the augmentation of both degradation in blood and hepatic uptake of the liposomes.
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