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Chinese Herbal Formula (CHF03) Attenuates Non-Alcoholic Fatty Liver Disease (NAFLD) Through Inhibiting Lipogenesis and Anti-Oxidation Mechanisms

机译:中草药配方(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)

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摘要

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-κB 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-κB, 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.
机译:非酒精性脂肪肝疾病(NAFLD)是一种肝脏疾病,在人群中发病率迅速上升,这在很大程度上归因于饮食中的营养过多和随后的肥胖症。发现针对NAFLD的有效天然化合物和草药可以为当前的化学药物提供替代和补充的医学治疗方法。在这项研究中,对ICR雄性小鼠进行体内高脂饮食(HFD)喂养,并在体外用棕榈酸(PA)处理AML12细胞。我们通过HE染色,透射电镜,Western印迹和基因表达,探讨中药CHF03对NAFLD的保护作用及其潜在机制。在体内,氧化应激标记(GSH,GSH-px,MDA,SOD和CAT)证实CHF03减轻了氧化应激和NF-κB蛋白的含量,表明炎症和氧化应激的降低。 ACACA和FASN的较低蛋白质丰度表明对脂肪生成有预防作用。组织学和超微结构观察表明,CHF03抑制NAFLD。 Srebf1,Fasn和Acaca,与脂肪形成相关的表达下调。在体外,基因和蛋白质以剂量依赖性方式表达,与肝脏中的一致。 CHF03抑制AML12细胞中脂质的积累和NF-κB的表达,核转移以及转录活性。通过改变脂肪形成基因的表达并减轻氧化应激,CHF03可能在预防肝脂肪变性中起有益作用。

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