Knockdown of hepatic aquaglyceroporin-9 alleviates high fat diet-induced non-alcoholic fatty liver disease in rats
Knockdown of hepatic aquaglyceroporin-9 alleviates high fat diet-induced non-alcoholic fatty liver disease in rats
复制标题
肝水甘油孔蛋白 9 的敲低可减轻高脂饮食诱导的大鼠非酒精性脂肪肝
DOI：
10.1016/j.intimp.2013.01.020
复制
发表时间：
2013-03-01
影响因子：
5.6
通讯作者：
Jiang, Zheng
中科院分区：
文献类型：
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作者：
Cai, Can;Wang, Chuan;Jiang, Zheng
非酒精性脂肪肝病 (NAFLD) 已成为一种常见的公共卫生问题，可进展为终末期肝病。尽管水甘油孔蛋白-9 (AQP9) 作为甘油通道的功能已被证实，但 AQP9 在 NAFLD 发展中的机制仍知之甚少。为了研究肝脏甘油摄取抑制的效果，我们利用慢病毒相关 RNA 干扰技术来敲低高脂饮食 (HFD) 诱导的啮齿动物 NAFLD 中肝脏 AQP9 的表达。雄性 Sprague Dawley 大鼠用标准饲料或 HFD 喂养 8 周。将HFD喂养的大鼠分为3组：HFD组、对照组和转染组，通过肝门静脉注射等量的PBS、慢病毒-scramble和慢病毒-shRNA-AQP9。结果显示转染组肝脏中AQP9 mRNA和蛋白的表达显着下降。此外，8周后与HFD组和对照组相比，肝脏脂肪变性发生较少。我们的结果表明 AQP9 在肝脂肪变性的发病机制中具有潜在作用。 (C) 2013 Elsevier B.V. 保留所有权利。
Non-alcoholic fatty liver disease (NAFLD) has emerged as a common public health problem that can progress to end-stage liver disease. Although the function of aquaglyceroporin-9 (AQP9) as a glycerol channel has been proven, the mechanism of AQP9 in the development of NAFLD is poorly understood. To investigate the effect of hepatic glycerol uptake inhibition, we utilized a lentivirus-associated RNA interference technique to knock down the expression of hepatic AQP9 in high fat diet (HFD)-induced NAFLD in rodents. Male Sprague Dawley rats were fed with a standard chow diet or HFD for 8 weeks. Rats fed a HFD were separated into 3 groups: HFD, control and transfection group, which were injected with equivalent amounts of PBS, lentivirus-scramble and lentivirus-shRNA-AQP9 through the hepatic portal vein. The results showed a remarkable decrease in the expression of AQP9 mRNA and protein in liver for the transfection group. Furthermore, less hepatic steatosis occurred when compared to the HFD and control groups after 8 weeks. Our results indicate a potential role for AQP9 in the pathogenesis of hepatic steatosis. (C) 2013 Elsevier B.V. All rights reserved.