The impact of uric acid treatment on mitochlondria morphology and function in a steatosis model of L-02 cells
IF 2.6
3区 农林科学
Q2 FOOD SCIENCE & TECHNOLOGY
W. Xiang, Shi Cheng, Yong Zhou, Sift Desk Journals Open Access Journals
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Abstract
Background and objectives: Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic diseases worldwide. Oxidative stress (OS) is a major contributor toward NAFLD development, while mitochondria play a central role in OS. Our previous study has shown that uric acid (UA), as a dual function metabolite, could alleviate OS. This study examined the impact of UA on mitochondria morphology and function in a model of steatosis using L-02 cells to explore the pathogenesis of NAFLD. Methods: The L‐02 hepatocyte cell line was used to develop a steatosis cell model via 0.3 mM oleic acid (OA) over 24 h, subsequently treated with uric acid (UA) dose of 5, 10, and 20 mg/dL for 24, 48, and 72 h, respectively. The fluorescence intensity of reactive oxygen species (ROS), apoptosis rate, and activity of Succinate dehydrogenase(SDH), cytochrome oxidas(CCO), and adenosine triphosphate(ATP) synthase in electron transport chain (ETC), as well as the content of ATP and 8-OH-dG were examined; ultrastructure was observed under an electron microscope. Results: Treatment with UA at a concentration of 5 and 10 mg/dL decreased the rate of ROS production, apoptosis, and 8-OH-dG concentration, while supporting ATP recovery, and SDH activity in the steatosis model cell. It also promoted lipid droplet metabolism; however, the recovery of mitochondria morphology was not obvious. Conclusions: Treatment with UA dose of 5 and 10 mg/dL could protect mitochondria from OS damage. Future research requires a more stable and effective model. keywords: electron transport chain, oxidative stress, nonalcoholic fatty liver disease Copy rights: © 2020 The Author(s). Published by Sift Desk Journals Group This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The impact of uric acid treatment on mitochlondria morphology and function in a steatosis model of L-02 cells Journal of Food Science & Technology (ISSN: 2472-6419) DOI: 10.25177/JFST.5.5.RA.10667 Research
尿酸处理对L-02细胞脂肪变性模型线粒体形态和功能的影响
背景和目的:非酒精性脂肪性肝病(NAFLD)是世界范围内最常见的慢性疾病之一。氧化应激(OS)是NAFLD发展的主要因素,而线粒体在OS中起核心作用。我们之前的研究表明,尿酸(UA)作为一种双重功能代谢物,可以缓解OS。本研究利用L-02细胞研究了UA对脂肪变性模型中线粒体形态和功能的影响,以探讨NAFLD的发病机制。方法:采用0.3 mM油酸(OA) 24 h培养L‐02肝细胞,随后分别用5、10和20 mg/dL尿酸(UA)处理24、48和72 h。检测各组细胞活性氧(ROS)荧光强度、细胞凋亡率、电子传递链(ETC)琥珀酸脱氢酶(SDH)、细胞色素氧化物(CCO)、三磷酸腺苷(ATP)合成酶活性以及ATP、8-OH-dG含量;电镜下观察超微结构。结果:浓度为5和10 mg/dL的UA降低了脂肪变性模型细胞中ROS的产生率、凋亡率和8-OH-dG浓度,同时支持ATP的恢复和SDH的活性。促进脂滴代谢;但线粒体形态恢复不明显。结论:UA剂量5和10 mg/dL可保护线粒体免于OS损伤。未来的研究需要一个更加稳定有效的模型。关键词:电子传递链,氧化应激,非酒精性脂肪肝版权:©2020作者。这是一篇在知识共享署名许可(http://creativecommons.org/licenses/by/4.0/)下发布的开放获取文章,该许可允许在任何媒介上不受限制地使用、分发和复制,只要原始作品被适当引用。尿酸处理对L-02细胞脂肪变性模型中线粒体形态和功能的影响食品科学与技术杂志(ISSN: 2472-6419) DOI: 10.25177/JFST.5.5.RA.10667研究
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