N-acetyl cysteine protects osteoblastic function from oxidative stress
N-acetyl cysteine protects osteoblastic function from oxidative stress
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DOI：
10.1002/jbm.a.33211
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发表时间：
2011-12-01
影响因子：
4.9
通讯作者：
Ogawa, T.
中科院分区：
文献类型：
--
作者：
Ueno, T.;Yamada, M.;Ogawa, T.
我们测试了一种抗氧化氨基酸衍生物n -乙酰半胱氨酸（NAC）在控制对成骨细胞的氧化应激中的保护潜力。从大鼠骨髓中提取成骨细胞进行培养。在培养基中加入100 μ M H(2)O(2)诱导氧化应激。然后，将H(2)O(2)处理过的培养物与2.5或5 mM NAC共处理。在第2天，H(2)O(2)的加入使细胞数量减少到未处理培养的50%。在H(2)O(2)培养物中加入5 mM NAC，细胞数量呈剂量依赖性增加，细胞数量比100 μ M H(2)O(2)培养物增加50%。H(2)O(2)作用后，第7天I型胶原蛋白、骨桥蛋白和骨钙素基因表达水平下调3倍。NAC共处理后，H(2)O(2)抑制基因的表达完全恢复。第15天Von Kossa染色评估，NAC + H(2)O(2)共处理组的矿化能力约为单独H(2)O(2)培养组的1.8倍。这些NAC介导的恢复与NAC剂量依赖性细胞内谷胱甘肽的增加和NAC剂量依赖性细胞内活性氧的减少有关。综上所述，氧化应激诱导的H(2)O(2)严重损害成骨细胞的增殖、分化和矿化。更重要的是，由于氧化还原平衡的改善，在培养物中添加NAC可以将这些损伤恢复到接近正常水平，这需要进一步的体内研究来测试其作为局部抗氧化应激药物的治疗潜力。(C) 2011 Wiley期刊公司[J] .中国生物医学工程学报，2011,31(1):531 -531。
We tested the protective potential of an antioxidant amino acid derivative, N-acetyl cysteine (NAC), in controlling oxidative stress against osteoblasts. Osteoblastic cells extracted from rat bone marrow were cultured. Oxidative stress was induced by adding 100 mu M H(2)O(2) into the culture media. Then, some H(2)O(2)-treated cultures were cotreated with 2.5 or 5 mM NAC. Addition of H(2)O(2) decreased the number of cells to 50% of untreated cultures at days 2. Addition of 5 mM NAC into H(2)O(2) cultures resulted in a dose-dependent increase in the number of cells, with the cell number being 50% greater than that in the 100 mu M H(2)O(2) culture. The gene expression levels of type I collagen, osteopontin, and osteocalcin were downregulated threefold by H(2)O(2) on day 7. The H(2)O(2)-suppressed gene expression was fully recovered by NAC cotreatment. The mineralizing capability, assessed by Von Kossa staining on day 15, were approximately 1.8 times greater in the NAC + H(2)O(2) cotreated group than in the culture with H(2)O(2) alone. These NAC-mediated restorations were associated with an NAC dose-dependent increase of intracellular glutathione and a NAC dose-dependent decrease of intracellular reactive oxygen species. In conclusion, oxidative stress induced by H(2)O(2) substantially impairs the proliferation, differentiation, and mineralization of osteoblasts. More importantly, the addition of NAC into the culture was found to restore these damages to a near normal level due to the improved redox balance, warranting further in vivo studies to test its therapeutic potential as a local antioxidative stress drug. (C) 2011 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 99A: 523-531, 2011.