Chinese Herbal Formula (CHF03) Attenuates Non-Alcoholic Fatty Liver Disease (NAFLD) Through Inhibiting Lipogenesis and Anti-Oxidation Mechanisms
Chinese Herbal Formula (CHF03) Attenuates Non-Alcoholic Fatty Liver Disease (NAFLD) Through Inhibiting Lipogenesis and Anti-Oxidation Mechanisms
复制标题
中药复方CHF03通过抑制脂肪生成和抗氧化机制减轻非酒精性脂肪性肝病（NAFLD）
DOI：
10.3389/fphar.2019.01190
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发表时间：
2019-10-15
影响因子：
5.6
通讯作者：
Xu, Chuang
中科院分区：
文献类型：
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作者：
Cui, Yizhe;Chang, Renxu;Xu, Chuang
非酒精性脂肪性肝病(NAFLD)是一种肝脏疾病，在人类人群中发病率迅速上升，主要原因是饮食过度营养和随后的肥胖。发现有效的天然化合物和草药对抗NAFLD可以为目前的化学药物提供替代和补充的医疗方法。本研究中，ICR雄性小鼠体内喂饲高脂饲料，体外用棕榈酸(PA)处理AML12细胞。通过HE染色、透射电子显微镜分析、Western blotting和基因表达等方法，探讨中药复方(CHF03)对NAFLD的保护作用及其可能的机制。在体内，氧化应激标志物(GSH、GSH-Px、MDA、SOD和CAT)证实CHF03减轻了氧化应激，并丰富了NF-kappa B蛋白，表明炎症和氧化应激有所减轻。ACACA和FASN蛋白丰度较低，提示对脂肪生成有预防作用。组织学和超微结构观察显示CHF03对NAFLD有抑制作用。与脂肪生成相关的Srebf1、FASN和AcacA的表达下调。在体外，基因和蛋白质以剂量依赖的方式表达，与肝脏中的表达一致。CHF03可抑制AML12细胞的脂质堆积和核因子-kappaB的表达、核移植和转录活性。CHF03可能通过改变造脂基因的表达，减轻氧化应激，从而在预防肝脏脂肪变性方面发挥有益的作用。
Nonalcoholic fatty liver disease (NAFLD) is a hepatic ailment with a rapidly increasing incidence in the human population due largely to dietary hyper nutrition and subsequent obesity. Discovering effective natural compounds and herbs against NAFLD can provide alternative and complementary medical treatments to current chemical pharmaceuticals. In this study, ICR male mice were fed a high-fat diet (HFD) in vivo and the AML12 cells were treated with palmitic acid (PA) in vitro. We explore the protective effect and potential mechanism of Chinese Herbal Formula (CHF03) against NAFLD by HE staining, transmission Electron Microscopy assay, Western blotting, and gene expression. In vivo, oxidative stress markers (GSH, GSH-px, MDA, SOD, and CAT) confirmed that CHF03 alleviated oxidative stress and abundance of NF-kappa B proteins indicating a reduction in inflammation and oxidative stress. The lower protein abundance of ACACA and FASN indicated a preventive effect on lipogenesis. Histological and ultrastructural observations revealed that CHF03 inhibited NAFLD. Expression of Srebf1, Fasn, and Acaca, which are associated with lipogenesis, were downregulated. In vitro, genes and proteins are expressed in a dose-dependent manner, consistent with those in the liver. CHF03 inhibited lipid accumulation and expression of NF-kappa B, nuclear transfer, and transcriptional activity in AML12 cells. The CHF03 might have a beneficial role in the prevention of hepatic steatosis by altering the expression of lipogenic genes and attenuating oxidative stress.