云芝多糖对小鼠腹腔巨噬细胞锰超氧化物歧化酶基因表达的调控  

The Regulation of Manganese Superoxide Dismutase Gene Expression in Mouse Peritoneal Macrophages by Polysaccharide Krestin

作　　者：庞战军[1] 陈瑗[1] 周玫[1] 

机构地区：[1]第一军医大学生物化学与分子生物学研究所自由基医学研究室

出　　处：《中国动脉硬化杂志》1999年第2期106-109,共4页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金

摘　　要：为揭示云芝多糖抗动脉粥样硬化的作用与细胞抗氧化酶的关系，采用酶活性测定、斑点杂交等方法，探讨了云芝多糖对小鼠腹腔巨噬细胞锰超氧化物歧化酶基因表达的影响。结果发现，腹腔注射云芝多糖可以提高小鼠腹腔巨噬细胞的总超氧化物歧化酶活性，从２２３．７±２９．１提高至３５６．１±９．３ｋｕ／ｇ，并使其锰超氧化物歧化酶ｍＲＮＡ含量增加；应用ＡｃｔｉｎｏｍｙｃｉｎＤ、Ｃｙｃｌｏｈｅｘｉｍｉｄｅ和Ａｃｅｔｏｖａｎｉｌｏｎｅ等阻断剂的研究发现，云芝多糖对巨噬细胞锰超氧化物歧化酶表达的影响发生在转录水平，而且某种新蛋白的合成可能参与了诱导过程。此结果提示，云芝多糖提高抗氧化酶活性，增强细胞抗氧化损伤的能力，可能是云芝多糖抗动脉粥样硬化作用机制之一。Aim In order to find out if the effect of polydaccharide Krestin (PSK) in preventing atherosclerosis is somewhat associated with antioxidant enzymes. Methods Applied pyrogallol auto-oxidatioon method to determine activity of superoxide dismutase (SOD). The content of manganese superoxide dismutase (MnSOD) mRNA in mouse peritoneal macrophages was detected through dot hybridization. Results It showed that, PSK could improve SOD activity from 223.7±29.1 to 356.1±9.3 ku/g (P<0.05) and increase the content of MnSOD mRNA in mouse peritoneal macrophages. And actinomycin D or cycloheximide could block the induction of MnSOD by PSK. Conclusion PSK could enhance SOD activity and MnSOD mRNA expression in mouse peritoneal macrophages. PSK might induce MnSOD mRNA transcription through a new protein synthesis pathway.

关 键 词：云芝多糖 SOD 基因表达 巨噬细胞 锰 

分 类 号：R285.5[医药卫生—中药学]