• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Human and Experimental Toxicology >Protective effects of casein-derived peptide VLPVPQK against hydrogen peroxide-induced dysfunction and cellular oxidative damage in rat osteoblastic cells
【24h】

Protective effects of casein-derived peptide VLPVPQK against hydrogen peroxide-induced dysfunction and cellular oxidative damage in rat osteoblastic cells

机译：酪蛋白衍生肽VLPVPQK对大鼠骨细胞致氢氧化功能障碍和细胞氧化损伤的保护作用

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Oxidative stress inhibits osteoblast differentiation and function that lead to the development of osteoporosis. Casein-derived peptide VLPVPQK (PEP), a potent antioxidant, was isolated from -casein of buffalo milk. We used an in vitro oxidative stress model induced by hydrogen peroxide (H2O2) in rat osteoblastic cells to investigate the protective effects of PEP against H2O2-induced dysfunction and oxidative damage. Cells were pretreated with PEP (50-200 ng/mL) for 2, 7 or 21 days followed by 0.3 mM H2O2 treatment for 24 h and then markers of osteogenic development, oxidative damage and apoptosis were examined. PEP significantly increased the viability and differentiation markers of osteoblast cells such as alkaline phosphatase and calcium mineralization. Moreover, PEP suppressed the production of reactive oxygen species (ROS), lipid peroxidation and ameliorated H2O2-induced reduction in glutathione, superoxide dismutase and catalase activities. In addition, PEP partially inhibited caspase-9 and-3 activities and reduced propidium iodide-positive cells. Altogether, our results demonstrated that PEP could protect rat osteoblast against H2O2-induced dysfunction and oxidative damage by reduction of ROS production, lipid peroxidation and increased antioxidant enzyme activities. Thus, our data suggest that PEP might be a valuable protective agent against oxidative stress-related diseases such as osteoporosis.
机译：氧化应激抑制了导致骨质疏松症的发展的成骨细胞分化和功能。酪蛋白衍生的肽VLPVPQK（PEP），一种有效的抗氧化剂，从水牛牛奶中分离出来。我们使用大鼠骨细胞中的过氧化氢（H 2 O 2）诱导的体外氧化应激模型，以研究PEP对H2O2诱导的功能障碍和氧化损伤的保护作用。将细胞用PEP（50-200ng / ml）预处理2,7或21天，然后进行0.3mM H 2 O 2处理24小时，然后检查成骨发育的标记，检查氧化损伤和细胞凋亡。 PEG显着增加了成骨细胞等活力和分化标志，如碱性磷酸酶和钙矿化。此外，PEP抑制了活性氧物质（ROS）的生产，脂质过氧化和改善的H2O2诱导的谷胱甘肽，超氧化物歧化酶和过氧化氢酶活性的降低。此外，PEP部分抑制了Caspase-9和-3活性和还原碘化丙啶阳性细胞。完全，我们的结果表明，通过降低ROS生产，脂质过氧化和抗氧化酶活性，PEP可以保护大鼠成骨细胞免受H2O2诱导的功能障碍和氧化损伤。因此，我们的数据表明，PEP可能是抗氧化应激相关疾病如骨质疏松症的有价值的保护剂。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号