Park Ji-Young, Cho Hye-Yeon, Kim Jong-Kyung, Noh Kyung-Hee, Yang Jeong-Rye, Ahn Jeong-Mi, Lee Mi-Ok, Song Young-Sun
School of Food and Life Science, Biohealth Product Research Center and Food Science Institute, Inje University, 607 Obang-dong, Kimhae 621-749, South Korea.
Clin Chim Acta. 2005 Jan;351(1-2):185-96. doi: 10.1016/j.cccn.2004.09.013.
It has been proposed that chlorella extracts have antioxidative and anti-inflammatory effects.
RAW 264.7 murine macrophage cell line was preincubated with various concentrations (0-100 mug/ml) of chlorella dichloromethane extract (CDE) and stimulated with lipopolysaccharide (LPS) to induce oxidative stress and inflammation.
Treatments of CDE reduced thiobarbituric acid-reactive substances (TBARS) accumulation, enhancing glutathione level and activities of antioxidative enzymes including superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-px), and glutathione reductase in LPS-stimulated macrophages than LPS-only treated cells. Nitric oxide (NO) production was significantly suppressed in a dose-dependent manner (p<0.05) with an IC(50) of 30.5 microg/ml. Treatment of CDE at 50 microg/ml suppressed NO production to 6% of LPS-control. Treatment with CDE suppressed the levels of inducible nitric oxide synthase (iNOS) protein and mRNA expressions. The specific DNA binding activities of nuclear factor kappa B (NF kappa B) on nuclear extracts from CDE treatments were significantly suppressed with an IC(50) of 62.7 mug/ml in a dose-dependent manner.
CDE ameliorates NO production and iNOS expression through the down-regulation of NF kappa B activity, which may be mediated by attenuated oxidative stress in RAW 264.7 macrophages.
有人提出小球藻提取物具有抗氧化和抗炎作用。
将RAW 264.7小鼠巨噬细胞系用不同浓度(0 - 100微克/毫升)的小球藻二氯甲烷提取物(CDE)预孵育,并用脂多糖(LPS)刺激以诱导氧化应激和炎症。
与仅用LPS处理的细胞相比,CDE处理可减少硫代巴比妥酸反应性物质(TBARS)的积累,提高谷胱甘肽水平以及包括超氧化物歧化酶(SOD)、过氧化氢酶、谷胱甘肽过氧化物酶(GSH-px)和谷胱甘肽还原酶在内的抗氧化酶的活性。一氧化氮(NO)的产生以剂量依赖性方式显著受到抑制(p<0.05),IC50为30.5微克/毫升。50微克/毫升的CDE处理可将NO产生抑制至LPS对照组的6%。CDE处理可抑制诱导型一氧化氮合酶(iNOS)蛋白水平和mRNA表达。CDE处理的细胞核提取物中核因子κB(NFκB)的特异性DNA结合活性以剂量依赖性方式显著受到抑制,IC50为62.7微克/毫升。
CDE通过下调NFκB活性改善NO产生和iNOS表达,这可能是由RAW 264.7巨噬细胞中氧化应激的减轻介导的。