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用柚皮苷预处理L6肌细胞可减轻氧化应激并增加葡萄糖摄取。

Preconditioning L6 Muscle Cells with Naringin Ameliorates Oxidative Stress and Increases Glucose Uptake.

作者信息

Dhanya R, Arun K B, Nisha V M, Syama H P, Nisha P, Santhosh Kumar T R, Jayamurthy P

机构信息

Agroprocessing and Natural Products Division, National Institute for Interdisciplinary Science and Technology (NIIST), CSIR, Industrial Estate, Pappanamcode, Thiruvananthapuram-695019, Kerala, India.

Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram-695012, Kerala, India.

出版信息

PLoS One. 2015 Jul 6;10(7):e0132429. doi: 10.1371/journal.pone.0132429. eCollection 2015.

Abstract

Enhanced oxidative stress contributes to pathological changes in diabetes and its complications. Thus, strategies to reduce oxidative stress may alleviate these pathogenic processes. Herein, we have investigated Naringin mediated regulation of glutathione (GSH) & intracellular free radical levels and modulation of glucose uptake under oxidative stress in L6 cell lines. The results from the study demonstrated a marked decrease in glutathione with a subsequent increase in free radical levels, which was reversed by the pretreatment of Naringin. We also observed that the increased malondialdehyde level, the marker of lipid peroxidation on induction of oxidative stress was retrieved on Naringin pretreatment. Addition of Naringin (100 μM) showed approximately 40% reduction in protein glycation in vitro. Furthermore, we observed a twofold increase in uptake of fluorescent labeled glucose namely 2-(N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)Amino)-2-Deoxyglucose (2-NBDG) on Naringin treatment in differentiated L6 myoblast. The increased uptake of 2-NBDG by L6 myotubes may be attributed due to the enhanced translocation of GLUT4. Our results demonstrate that Naringin activate GSH synthesis through a novel antioxidant defense mechanism against excessive Reactive Oxygen Species (ROS) production, contributing to the prevention of oxidative damage in addition to its effect on glycemic control.

摘要

氧化应激增强会导致糖尿病及其并发症的病理变化。因此,降低氧化应激的策略可能会减轻这些致病过程。在此,我们研究了柚皮苷在L6细胞系氧化应激条件下对谷胱甘肽(GSH)和细胞内自由基水平的调节作用以及对葡萄糖摄取的影响。研究结果表明,谷胱甘肽显著减少,随后自由基水平升高,而柚皮苷预处理可逆转这种情况。我们还观察到,在氧化应激诱导下作为脂质过氧化标志物的丙二醛水平升高,经柚皮苷预处理后恢复正常。添加柚皮苷(100 μM)在体外显示蛋白质糖基化减少约40%。此外,我们观察到在分化的L6成肌细胞中,经柚皮苷处理后,荧光标记葡萄糖即2-(N-(7-硝基苯并-2-恶唑-1,3-二氮杂环丁烷-4-基)氨基)-2-脱氧葡萄糖(2-NBDG)的摄取增加了两倍。L6肌管对2-NBDG摄取的增加可能归因于GLUT4转运的增强。我们的结果表明,柚皮苷通过一种新的抗氧化防御机制激活GSH合成,以对抗过量活性氧(ROS)的产生,除了对血糖控制有影响外,还有助于预防氧化损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b321/4492986/e29c6a0aa67e/pone.0132429.g001.jpg

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