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首页> 外文期刊>RSC Advances >Rosmarinic acid attenuates hepatic steatosis by modulating ER stress and autophagy in oleic acid-induced HepG2 cells
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Rosmarinic acid attenuates hepatic steatosis by modulating ER stress and autophagy in oleic acid-induced HepG2 cells

机译：迷迭香酸通过调节内质网应激和自噬在油酸诱导的HepG2细胞中减轻肝脂肪变性

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Non-alcoholic fatty acid disease (NAFLD) has become an emerging entity of liver disorders worldwide. Oxidative stress and deranged autophagy-induced endoplasmic reticulum (ER) stress has recently been recognized as one of the prime factors involved in the pathological mechanism underlying NAFLD and progressive non-alcoholic steato-hepatitis (NASH). Epidemiological and experimental data reveal the potency of dietary polyphenols in averting NAFLD. In this line, to analyse and address the underlying pathogenic mechanisms, in the present study, oleic acid-induced HepG2 cells were treated with rosmarinic acid (RA), a dietary polyphenol with well-established cytoprotective properties. Treatment with rosmarinic acid (20 μg) was found to potently counter the elevated levels of total cholesterol (TC) and triglycerides (TG). Additionally, exposure of oleic acid-induced HepG2 cells to rosmarinic acid showed reduced levels of ROS and increased activity of enzymic and non-enzymic antioxidants. The steatotic HepG2 cells presented a pronounced increase in the expression of key ER stress markers such as p-PERK, p-IRE-1, ATF-6, p-eIF-α and CHOP, which was considerably reduced upon treatment with rosmarinic acid. Moreover, exposure to rosmarinic acid altered the deranged autophagic mechanism in oleic acid-induced HepG2 cells, which was observed via the protein expression of Beclin 1, LC31, ATG5 and ATG7. This study demonstrates that rosmarinic acid abrogates NAFLD via diminishing ER stress by nullifying oxidative stress and restoring deranged autophagy and can be used as a potent adjunct in the treatment of NAFLD, thus illustrating the valuable application of polyphenols in combating NAFLD.
机译：非酒精性脂肪酸疾病（NAFLD）已成为全球肝脏疾病的新兴实体。氧化应激和自噬引起的内质网（ER）紊乱最近被认为是导致NAFLD和进行性非酒精性脂肪性肝炎（NASH）的病理机制的主要因素之一。流行病学和实验数据表明，饮食中的多酚可有效避免NAFLD。在这一方面，为了分析和解决潜在的致病机理，在本研究中，油酸诱导的HepG2细胞用迷迭香酸（RA）（一种具有良好细胞保护特性的饮食多酚）处理。发现用迷迭香酸（20μg）处理可有效抵消总胆固醇（TC）和甘油三酸酯（TG）升高的水平。此外，油酸诱导的HepG2细胞暴露于迷迭香酸中可降低ROS水平，并提高酶和非酶抗氧化剂的活性。脂肪变性的HepG2细胞在关键ER应激标志物（例如p-PERK，p-IRE-1，ATF-6，p-eIF-α和CHOP）的表达上有明显增加，在用迷迭香酸处理后，这种表达大大降低了。此外，暴露于迷迭香酸改变了油酸诱导的HepG2细胞中自噬的紊乱机制，这是通过Beclin 1，LC31，ATG5和ATG7的蛋白表达观察到的。这项研究表明，迷迭香酸通过消除氧化应激和恢复紊乱的自噬，通过降低内质网应激来消除NAFLD，并且可以用作NAFLD的有效辅助剂，从而说明了多酚在对抗NAFLD中的有价值的应用。

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