枯否细胞在小鼠体内可溶性抗肿瘤（1→3）-β-D-葡聚糖SSG的代谢降解过程中发挥着重要作用。

Kupffer cells play important roles in the metabolic degradation of a soluble anti-tumor (1-->3)-beta-D-glucan, SSG, in mice.

作者信息

Suda M, Ohno N, Hashimoto T, Koizumi K, Adachi Y, Yadomae T

机构信息

Laboratory of Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science, Japan.

出版信息

FEMS Immunol Med Microbiol. 1996 Sep;15(2-3):93-100. doi: 10.1111/j.1574-695X.1996.tb00058.x.

DOI:10.1111/j.1574-695X.1996.tb00058.x

PMID:8880133

Abstract

Metabolic degradation of a soluble highly branched (-->3)-beta-D-glucan, SSG, was examined in mice using a macrophage blocker, gadolinium chloride (GdCl3). Intraperitoneally administered SSG distributed in the liver was slowly degraded, and after 5 weeks about 30% of the SSG became anionic. In addition, it is suggested that the metabolites would contain fewer branching points as assessed by the reactivity to limulus factor G. On the other hand, in the spleen, the molecular weight and the degree of branching of SSG were not changed for at least 5 weeks. Blockade of Kupffer cells by GdCl3 did not significantly change the distribution ratio of SSG in the liver. However, the treatment significantly delayed the degradation of SSG. These results suggested that Kupffer cells play important roles, not in the distribution, but in the oxidative degradation of SSG in the liver. In addition, splenic macrophages did not significantly contribute to the metabolic degradation of SSG.

摘要

使用巨噬细胞阻断剂氯化钆（GdCl₃）在小鼠体内研究了可溶性高度分支的（→3）-β-D-葡聚糖（SSG）的代谢降解情况。腹腔注射后，分布于肝脏的SSG降解缓慢，5周后约30%的SSG变为阴离子型。此外，根据对鲎试剂G的反应性评估，提示代谢产物的分支点会减少。另一方面，在脾脏中，SSG的分子量和分支程度至少5周内未发生变化。GdCl₃对枯否细胞的阻断并未显著改变SSG在肝脏中的分布比例。然而，该处理显著延迟了SSG的降解。这些结果表明，枯否细胞在肝脏中对SSG的氧化降解而非分布起重要作用。此外，脾巨噬细胞对SSG的代谢降解贡献不大。