...
首页> 外文期刊>Biomedicine & pharmacotherapy =: Biomedecine & pharmacotherapie >Antioxidant effects of Lycium barbarum polysaccharides on photoreceptor degeneration in the light-exposed mouse retina
【24h】

Antioxidant effects of Lycium barbarum polysaccharides on photoreceptor degeneration in the light-exposed mouse retina

机译:枸杞多糖对曝光小鼠视网膜光感受器变性的抗氧化作用

获取原文
获取原文并翻译 | 示例
           

摘要

We assessed the neuroprotective effects of Lycium barbarum Polysaccharides (LBP) on photoreceptor degeneration and the mechanisms involved in oxidative stress in light-exposed mouse retinas. Mice were given a gavage of LBP (150 mg/kg or 300 mg/kg) or phosphate buffered saline (PBS) for 7 days before exposure to light (5000 lx for 24 h). We found that LBP significantly improved the electroretinography (ERG) amplitudes of the aand b-waves that had been attenuated by light exposure. In addition, changes caused by light exposure including photoreceptor cell loss, nuclear condensation, an increased number of mitochondria vacuoles, outer membrane disc swelling and cristae fractures were distinctly ameliorated by LBP. LBP treatment also significantly prevented the generation of reactive oxygen species (ROS) compared with PBS treatment. The levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and thioredoxin reductase (TrxR1) mRNA were decreased in PBS-treated mice compared with controls but increased remarkably in LBP-treated mice. The mRNA levels of the DNA repair gene Poly (ADP-ribose) polymerase (PARP14) was increased in PBS-treated mice but decreased significantly in the LBP-treated mice. Our findings indicate that pretreatment with LBP effectively protected photoreceptor cells against light-induced retinal damage probably through the up-regulation of the antioxidative genes Nrf2 and TrxR1, the elimination of oxygen free radicals, and the subsequent reduction in the mitochondrial reaction to oxidative stress and enhancement in antioxidant capacity. In addition, the decreased level of PARP14 mRNA in LBP-treated mice also indicated a protective effect of LBP on delaying photoreceptor in the light-damaged retina.
机译:我们评估了枸杞多糖(LBP)对感光体变性的神经保护作用及氧化胁迫在暴露的小鼠视黄糖中的机制。在暴露于光(5000 Lx 24小时)之前,将小鼠施用LBP(150mg / kg或300mg / kg)或磷酸盐缓冲盐水(PBS)7天。我们发现LBP显着改善了通过光曝光而衰减的AAND B波的电型造稿(ERG)幅度。此外,LBP明显改善了由光曝光细胞损失,核缩合,线粒体裂缝,外膜盘肿胀和嵴裂缝的核凝结,核凝结增加。与PBS处理相比,LBP处理也显着地防止了活性氧物质(ROS)的产生。与对照相比,PBS处理的小鼠中,核因子红细胞2相关因子2(NRF2)和硫辛素还原酶(TRXR1)mRNA的水平降低,但在LBP处理的小鼠中显着增加。 DNA修复基因聚(ADP-核糖)聚合酶(PARP14)的mRNA水平在PBS处理的小鼠中增加,但在LBP处理的小鼠中显着降低。我们的研究结果表明,LBP的预处理有效地保护光感受器细胞免受光诱导的视网膜损伤,可能是通过抗氧化基因NRF2和TRXR1的上调,消除氧自由基,以及随后的线粒体反应对氧化应激的影响增强抗氧化能力。此外,LBP处理小鼠中PARP14 mRNA的降低也表明LBP对延迟光感受器在浅损伤视网膜中的保护作用。

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