...
首页> 外文期刊>International Journal of Food Sciences and Nutrition >Mulberry leaf phenolics ameliorate hyperglycemia-induced oxidative stress and stabilize mitochondrial membrane potential in HepG2 cells
【24h】

Mulberry leaf phenolics ameliorate hyperglycemia-induced oxidative stress and stabilize mitochondrial membrane potential in HepG2 cells

机译:桑椹叶酚类改善高血糖诱导的氧化胁迫并稳定HepG2细胞中的线粒体膜电位

获取原文
获取原文并翻译 | 示例

摘要

To investigate the effect of phenolics in mulberry leaves (mulberry leaf phenolics; MLP) on hyperglycemia-induced oxidative stress and mitochondrial membrane potential (Delta Psi m) in HepG2 cells; we treated HepG2 with glucose [5.5 (N-Glc) or 50 mmol/L (Hi-Glc)] with or without MLP at 10 or 100 mmol/L gallic acid equivalents and assessed level of reactive oxidant species (ROS), Delta Psi m, malondialdehyde (MDA) and nuclear factor-kappaB (NF-kappa B) activation. Hi-Glc-induced oxidative damage was demonstrated by a series of increase in superoxides (560%, 0.5 h), MDA (400%, 24 h), NF-kappa B activation (474%, 4 h) and a wild fluctuation of Delta Psi m relative to the control cells (p <= 0.05). MLP treatments ameliorate Hi-Glc-induced negative effects by a 40% reduction in ROS production, 34-44% reduction in MDA production, over 35% inhibition of NF-kappa B activation, as well as exert protective effect on HepG2 cells from change in Delta Psi m. Our data show that MLP in vitro can protect hepatoctyes from hyperglycemia-induced oxidative damages.
机译:探讨苯酚中酚醛叶(桑叶酚类; MLP)对高血糖诱导的氧化胁迫和线粒体膜电位(Delta psi m)的影响;我们用葡萄糖[5.5(n-glc)或50mmol / l(Hi-glc)]治疗hepg2,或没有MLP,在10或100mmol / L Gallic酸等当量和评估水平的反应氧化物种(ROS),Delta psi M,丙二醛(MDA)和核因子 - κB(NF-Kappa B)活化。通过一系列超氧化物(560%,0.5小时),MDA(400%,24小时),NF-κB活化(474%,4小时)和野生波动的一系列增加证明了Hi-Glc诱导的氧化损伤。 Delta psi m相对于对照细胞(p <= 0.05)。 MLP治疗改善Hi-Glc诱导的负面影响,降低ROS生产的40%,MDA生产降低34-44%,抑制NF-Kappa B激活超过35%,以及对HepG2细胞的影响免受变化的保护作用在delta psi m。我们的数据显示,MLP体外可以保护Hepatocty来自高血糖诱导的氧化损伤。

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