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首页> 外文期刊>Journal of orthopaedic research >Fullerol antagonizes dexamethasone-induced oxidative stress and adipogenesis while enhancing osteogenesis in a cloned bone marrow mesenchymal stem cell
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Fullerol antagonizes dexamethasone-induced oxidative stress and adipogenesis while enhancing osteogenesis in a cloned bone marrow mesenchymal stem cell

机译：富勒醇拮抗地塞米松诱导的氧化应激和脂肪生成，同时增强克隆的骨髓间充质干细胞的成骨作用

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Increased oxidative stress is currently considered as a crucial cause of corticosteroid-induced osteonecrosis. The aim of this study was to evaluate the effect of fullerol, a powerful antioxidant, on adipogenic and osteogenic differentiation of a mouse bone marrow derived multipotent cell line, D1. Upon treatment with dexamethasone, D1 cells containing lipid vesicles were distinguishable from the surrounding cells by Oil Red O staining at day 21. Simultaneous treatment of dexamethasone with antioxidant glutathione or fullerol decreased the number of cells containing lipid vesicles. Treatment with dexamethasone for 7 days resulted in a significant increase in adipogenic markers peroxisome proliferator-activated receptor gamma and adipocyte protein 2 gene expression and decrease in expression of osteogenic markers runt-related transcription factor 2 and osteocalcin and antioxidative enzymes superoxide dismutase and catalase as revealed by quantitative real-time PCR. While glutathione and fullerol both were able to antagonize the effects of dexamethasone, fullerol had a greater effect than glutathione. Staining with a fluorescent dye CM-H 2DCFDA as indicator of cellular reactive oxygen species revealed that the percentage of positively stained cells increased after dexamethasone treatment, and addition of fullerol attenuated this activity. These results indicated that fullerol inhibited adipogenesis and simultaneously enhanced osteogenesis by marrow mesenchymal stem cells possibly through elimination of cellular reactive oxygen species. The results indicated that fullerol can potentially be used for prevention and treatment of corticosteroid-induced osteonecrosis.
机译：目前认为氧化应激增加是皮质类固醇诱导的骨坏死的关键原因。这项研究的目的是评估富勒醇（一种强大的抗氧化剂）对小鼠骨髓衍生的多能细胞系D1成脂和成骨分化的影响。用地塞米松治疗后，在第21天通过油红O染色将含有脂质囊泡的D1细胞与周围细胞区分开。同时用抗氧化剂谷胱甘肽或富勒醇同时处理地塞米松减少了含有脂质囊泡的细胞数量。地塞米松治疗7天导致脂肪生成标记过氧化物酶体增殖物激活的受体γ和脂肪细胞蛋白2基因表达显着增加，成骨标记矮子相关转录因子2和骨钙素及抗氧化酶超氧化物歧化酶和过氧化氢酶的表达降低通过定量实时PCR。尽管谷胱甘肽和富勒醇都能拮抗地塞米松的作用，但富勒醇的作用要比谷胱甘肽更大。用荧光染料CM-H 2DCFDA染色作为细胞活性氧种类的指标，显示地塞米松处理后阳性染色细胞的百分比增加，而富勒醇的加入减弱了该活性。这些结果表明，富勒醇可能通过消除细胞中的活性氧而抑制了骨髓间充质干细胞的脂肪生成并同时增强了成骨作用。结果表明，富勒醇可潜在地用于预防和治疗皮质类固醇诱发的骨坏死。

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