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来自……的一个组分可改善小鼠模型中的肝脂肪变性。 (你提供的原文不完整,此译文是根据现有内容尽量完整翻译的,完整准确的翻译需结合完整原文)

, a Fraction From , Ameliorates Hepatic Steatosis in Mice Models.

作者信息

Yi Qin, Sun Puyang, Li Juan, Kong Siming, Tian Jinying, Li Xuechen, Yang Yanan, Zhang Peicheng, Liu Yuying, Han Jingyan, Zhang Xiaolin, Ye Fei

机构信息

Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study, Institute of Materia Medica, Chinese Academy of Medical Science & Peking Union Medical College, Beijing, China.

State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Science & Peking Union Medical College, Beijing, China.

出版信息

Front Physiol. 2018 Mar 14;9:222. doi: 10.3389/fphys.2018.00222. eCollection 2018.

Abstract

The prevalence of non-alcoholic fatty liver disease (NAFLD), which is developed from hepatic steatosis, is increasing worldwide. However, no specific drugs for NAFLD have been approved yet. To observe the effects of , a fraction from , on non-alcoholic hepatic steatosis, three mouse models with characteristics of NAFLD were used including high-fat diet (HFD)-induced obesity (DIO) mice, KKAy mice, and HFD combined with tetracycline stimulated Model-T mice. Hepatic lipid accumulation was determined via histopathological analysis and/or hepatic TG determination. The responses to insulin were evaluated by insulin tolerance test (ITT), glucose tolerance test (GTT), and hyperinsulinemic-euglycemic clamp, respectively. The pathways involved in hepatic lipid metabolism were observed via western-blot. Furthermore, the liver microcirculation was observed by inverted microscopy. The HPLC analysis indicated that the main components of were flavan polymers. The results of histopathological analysis showed that could ameliorate hepatic steatosis in DIO, KKAy, and Model-T hepatic steatosis mouse models, respectively. After treatment in DIO mice, insulin resistance was improved with increasing glucose infusion rate (GIR) in hyperinsulinemic-euglycemic clamp, and decreasing areas under the blood glucose-time curve (AUC) in both ITT and GTT; the pathways involved in fatty acid uptake and lipogenesis were both down-regulated, respectively. However, the pathways involved in beta-oxidation and VLDL-export on hepatic steatosis were not changed significantly. The liver microcirculation disturbances were also improved by in DIO mice. These results suggest that is a lead nature product for hepatic steatosis treatment. The mechanism is related to enhancing insulin sensitivity, suppressing fatty acid uptake and inhibiting lipogenesis in liver.

摘要

非酒精性脂肪性肝病(NAFLD)由肝脂肪变性发展而来,在全球范围内的患病率正在上升。然而,目前尚无获批用于治疗NAFLD的特效药物。为了观察[具体物质](一种从[具体来源]提取的组分)对非酒精性肝脂肪变性的影响,研究使用了三种具有NAFLD特征的小鼠模型,包括高脂饮食(HFD)诱导的肥胖(DIO)小鼠、KKAy小鼠以及HFD联合四环素刺激的Model-T小鼠。通过组织病理学分析和/或肝脏甘油三酯(TG)测定来确定肝脏脂质蓄积情况。分别通过胰岛素耐量试验(ITT)、葡萄糖耐量试验(GTT)和高胰岛素-正葡萄糖钳夹试验评估对胰岛素的反应。通过蛋白质免疫印迹法观察肝脏脂质代谢相关通路。此外,利用倒置显微镜观察肝脏微循环。高效液相色谱(HPLC)分析表明,[具体物质]的主要成分是黄烷聚合物。组织病理学分析结果显示,[具体物质]可分别改善DIO、KKAy和Model-T肝脂肪变性小鼠模型的肝脂肪变性。在DIO小鼠中给予[具体物质]治疗后,高胰岛素-正葡萄糖钳夹试验中随着葡萄糖输注速率(GIR)增加胰岛素抵抗得到改善,ITT和GTT中血糖-时间曲线下面积(AUC)均降低;脂肪酸摄取和[具体过程]脂肪生成相关通路均分别下调。然而,肝脂肪变性中β-氧化和极低密度脂蛋白(VLDL)输出相关通路未发生显著变化。[具体物质]还改善了DIO小鼠的肝脏微循环障碍。这些结果表明,[具体物质]是治疗肝脂肪变性的潜在天然产物。其作用机制与增强胰岛素敏感性、抑制脂肪酸摄取以及抑制肝脏[具体过程]脂肪生成有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978f/5861213/19565f3a07a0/fphys-09-00222-g0001.jpg

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