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首页> 外文期刊>Drug Design, Development and Therapy >Liraglutide Improves Non-Alcoholic Fatty Liver Disease In Diabetic Mice By Modulating Inflammatory Signaling Pathways
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Liraglutide Improves Non-Alcoholic Fatty Liver Disease In Diabetic Mice By Modulating Inflammatory Signaling Pathways

机译：Liraglutide通过调节炎症信号通路来改善糖尿病小鼠的非酒精脂肪肝疾病

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Background: Many chronic metabolic diseases, such as obesity and type 2 diabetes (T2DM), are closely related to a chronic low-grade inflammatory state in tissues. The high prevalence of non-alcoholic fatty liver disease (NAFLD) in patients with T2DM is related to the role of inflammation in the disease. In this study, we investigated the role of liraglutide in improving lipid metabolism disorders and preventing their progression to NAFLD by modulating inflammatory signaling pathways, thereby providing new treatment options for NAFLD. Methods: We designed a 2×2 factorial analysis experiment. A mouse model of NAFLD with T2DM was established by feeding the animals a high-fat diet (HFD). The NAFLD mice with HFD-induced diabetes were treated with liraglutide for 10 weeks. Hematoxylin and eosin staining, Oil Red O staining and electron microscopy were used to observe the accumulation of triglycerides in the liver. RT-PCR and Western blotting were used to analyze the expression of α-SMA, IL-1β, TNF-α, NF-κB and the NF-κB inhibitory protein IκB in the liver at the gene and protein levels, respectively. Results: Liraglutide reduced the body weight and fasting blood glucose levels of HFD-fed mice. The expression of α-SMA, IL-1β, TNF-α, and NF-κB in the liver of HFD-fed mice was increased at the mRNA and protein levels, but liraglutide treatment decreased the expression of these molecules. The expression of IκB in the liver decreased at the mRNA and protein levels but was upregulated after liraglutide treatment. Conclusion: Based on the current findings, liraglutide can significantly improve hepatic steatosis, primarily by downregulating the expression of inflammatory signaling mediators in the TNF-α pathway.
机译：背景：许多慢性代谢疾病，如肥胖症和2型糖尿病（T2DM），与组织中的慢性低级炎症状态密切相关。 T2DM患者的非酒精性脂肪肝疾病（NAFLD）的高患病率与炎症在疾病中的作用有关。在这项研究中，我们通过调节炎症信号传导途径来调查Liraglutide在改善脂质代谢紊乱并预防其对NAFLD的作用，从而为NAFLD提供新的治疗选择。方法：我们设计了一个2×2因子分析实验。通过将动物喂养高脂饮食（HFD）来建立具有T2DM的NAFLD的小鼠模型。具有HFD诱导的糖尿病的NAFLD小鼠用Liraglutide处理10周。苏木精和曙红染色，油红O染色和电子显微镜用于观察肝脏中甘油三酯的积累。 RT-PCR和Western印迹分别用于分析基因和蛋白质水平的α-SMA，IL-1β，TNF-α，NF-κB和NF-κB抑制蛋白IκB的表达。结果：Liraglutide降低了HFD喂养小鼠的体重和空腹血糖水平。在mRNA和蛋白质水平上增加了α-SMA，IL-1β，TNF-α和NF-κB的表达，但林林肽处理降低了这些分子的表达。肝脏中IκB的表达在mRNA和蛋白质水平下降，但在黎勒德德治疗后被上调。结论：基于目前的调查结果，Liraglutide可以显着改善肝脏脂肪变性，主要是下调TNF-α途径中炎症信号介质的表达。

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