壳寡糖缓解甲萘醌诱导巨噬细胞损伤机制初探  

Effects of Chitosan Oligosaccharides Attenuating Menadione-induced Injury in Macrophages

作　　者：麻攀[1,2] 刘洪涛[1,2] 许青松[1] 白雪芳[1] 杜昱光[1] 

机构地区：[1]中国科学院大连化学物理研究所,大连116023 [2]中国科学院研究生院,北京100049

出　　处：《中国生物工程杂志》2011年第6期18-21,共4页China Biotechnology

基　　金：国家科技重大专项课题资助项目(2009ZX09501-011)

摘　　要：目的:研究壳寡糖对甲萘醌诱导的巨噬细胞氧化损伤的保护作用。方法:通过MTT实验检测相应处理的细胞活力,并通过相应试剂盒检测细胞氧化还原体系中某些相关酶的活力及相应产物含量。结果:壳寡糖能够缓解甲萘醌诱导的细胞损伤,并且发现壳寡糖可以缓解甲萘醌导致的胞内超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-PX)活力的降低,以及抑制相应的脂质过氧化反应产物(MDA)的产生,表明壳寡糖可能通过此机制来抵制甲萘醌导致的氧化损伤。结论:壳寡糖可以缓解甲萘醌诱导的细胞氧化损伤。Aim： To investigate the effects of Chitosan oligosaccharides （COS） on attenuating menadioneinduced stress injury in macrophages. Method： MTF assay was used to examine the cell viability, and the reagent kits were used to investigate the activities of enzymes and the products of lipid peroxidation in redox system. Results： By using MTY assay and detecting the activities of LDH （lactate dehydrogenase ） in the cultural supernatants, it was confirmed that chitosan oligosaccharides could attenuate menadione-induced stress injury in macrophages. Moreover, the results showed that COS could also restore activities of endogenous antioxidants including superoxide dismutase （SOD） and glutathione peroxidase （GSH-PX）, and suppressing the production of lipid peroxidation. Those results could explain the mechanisms of COS on attenuating menadione-induced stress injury in macrophages. Conclusion： Stress injury induced by menadione in macrophages could be blocked by COS.

关 键 词：壳寡糖 巨噬细胞 氧化应激 

分 类 号：Q819[生物学—生物工程]