Department of Gastroenterology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
Hepatobiliary Pancreat Dis Int. 2013 Dec;12(6):630-6. doi: 10.1016/s1499-3872(13)60099-5.
Non-alcoholic fatty liver disease (NAFLD) is one of the most frequent causes of liver diseases, with markedly increased prevalence. However, its mechanisms are not clear. The present study was undertaken to illustrate the role of caveolin-1 (cav1) and the scavenger receptor class B type 1 (SR-B1) in NAFLD.
Adult male C57BL/6 mice were fed with a normal diet or high fat and cholesterol (HFC) diet for 14 weeks. The mice were sacrificed to collect plasma and harvest the liver; their plasma lipid concentration was measured. Hepatic cav1 and SR-B1 mRNA and protein expression were determined by real-time quantitative polymerase chain reaction (qPCR) and Western blotting, respectively. In order to study cav1 and SR-B1 distribution and change in hepatocytes, immunohistochemical analysis was performed.
HFC diet increased plasma lipids, induced NAFLD and increased the liver/body weight ratio. Compared to the control mice (n=6), the mRNA and protein levels of cav1 and SR-B1 in liver tissue of the NAFLD mice (n=12) increased significantly (cav1 mRNA: 1.536+/-0.226 vs 0.980+/-0.272, P<0.05; protein: 0.643+/-0.240 vs 0.100+/-0.130, P<0.01; SR-B1 mRNA: 1.377+/-0.125 vs 0.956+/-0.151, P<0.01; protein: 2.156+/-0.507 vs 0.211+/-0.211, P<0.01). Furthermore, both cav1 and SR-B1 immunoreactivity increased and their distribution was also changed, mainly in the plasma membrane of hepatocytes, cytoplasm and membrane of lipid droplets and around.
NAFLD is associated with increased concentration of plasma lipids and upregulation of hepatic cav1 and SR-B1 gene and protein expressions, which indicate that cav1 and SR-B1 might play crucial roles in the pathogenesis of NAFLD.
非酒精性脂肪性肝病（NAFLD）是最常见的肝病病因之一，其发病率显著增加。然而，其发病机制尚不清楚。本研究旨在阐明窖蛋白-1（cav1）和清道夫受体 B 类 1 型（SR-B1）在 NAFLD 中的作用。
成年雄性 C57BL/6 小鼠给予正常饮食或高脂肪和胆固醇（HFC）饮食 14 周。处死小鼠收集血浆并采集肝脏；检测其血浆脂质浓度。采用实时定量聚合酶链反应（qPCR）和 Western blot 分别检测肝组织中 cav1 和 SR-B1mRNA 和蛋白的表达。为了研究 cav1 和 SR-B1 在肝细胞中的分布和变化，进行了免疫组织化学分析。
HFC 饮食增加了血浆脂质，诱导了 NAFLD，并增加了肝/体重比。与对照组小鼠（n=6）相比，NAFLD 小鼠（n=12）肝组织中 cav1 和 SR-B1 的 mRNA 和蛋白水平显著升高（cav1mRNA：1.536±0.226 比 0.980±0.272，P<0.05；蛋白：0.643±0.240 比 0.100±0.130，P<0.01；SR-B1mRNA：1.377±0.125 比 0.956±0.151，P<0.01；蛋白：2.156±0.507 比 0.211±0.211，P<0.01）。此外，cav1 和 SR-B1 的免疫反应性均增加，其分布也发生改变，主要位于肝细胞的质膜、细胞质和脂滴的膜以及周围。
NAFLD 与血浆脂质浓度升高以及肝 cav1 和 SR-B1 基因和蛋白表达上调有关，提示 cav1 和 SR-B1 可能在 NAFLD 的发病机制中起关键作用。
