You Yanting, Zhang Yuxing, Lu Yuanyuan, Hu Keke, Qu Xiaohu, Liu Yongzhag, Lu Bin, Jin Liqin
Key Laboratory of Laboratory Medicine, Ministry of Education, and Zhejiang Provincial Key Laboratory of Medical Genetics, Wenzhou Medical University, Wenzhou, Zhejiang 325035, P.R. China.
Mol Med Rep. 2017 Sep;16(3):2379-2388. doi: 10.3892/mmr.2017.6893. Epub 2017 Jun 30.
Mitochondrial dysfunction is closely associated with the pathogenesis of nonalcoholic steatohepatitis (NASH). The aim of the present study was to comprehensively determine mitochondrial abnormalities in NASH by detecting the proteomics in liver mitochondria in a NASH rat model, which was induced for 16 weeks by the provision of a high fat and high cholesterol diet (HFD). Serum parameters, including triglycerides, total cholesterol, low‑density lipoprotein cholesterol and high‑density lipoprotein cholesterol were determined, and hematoxylin and eosin staining of liver tissues was examined to evaluate the NASH rat model. Various parameters associated with mitochondrial function were examined, including mitochondrial DNA (mtDNA) copy number, mitochondrial membrane potential (MMP) and mitochondrial respiratory chain complex (MRC) activity. The mitochondrial proteomics were analyzed and identified using isobaric tags for relative and absolute quantitation labeling coupled with two‑dimensional liquid chromatography‑tandem mass spectrometry. The identified proteins were classified and grouped using the Blast2GO program against the non‑redundant protein database, the Kyoto Encyclopedia of Genes and Genomes database and the Cluster of Orthologous Groups of proteins database. Compared with the control, mtDNA copy number, MMP, and activities of MRC I and III were decreased markedly in the HFD group. A total of 18 upregulated and 13 downregulated proteins were identified, with a significant 1.2‑fold difference between the control and NASH groups. The dysregulated proteins were closely involved in mitochondrial oxidative phosphorylation, the lipid metabolic process and fatty acid β‑oxidation. The results of the present study provide important proteomic information regarding liver mitochondria in NASH and serve as a basis for further detailed investigations of the pathogenesis of NASH.
线粒体功能障碍与非酒精性脂肪性肝炎(NASH)的发病机制密切相关。本研究的目的是通过检测NASH大鼠模型肝线粒体中的蛋白质组学,全面确定NASH中线粒体的异常情况,该模型通过给予高脂肪高胆固醇饮食(HFD)诱导16周。测定血清参数,包括甘油三酯、总胆固醇、低密度脂蛋白胆固醇和高密度脂蛋白胆固醇,并检查肝组织的苏木精和伊红染色以评估NASH大鼠模型。检测了与线粒体功能相关的各种参数,包括线粒体DNA(mtDNA)拷贝数、线粒体膜电位(MMP)和线粒体呼吸链复合体(MRC)活性。使用相对和绝对定量标记的等压标签结合二维液相色谱-串联质谱对线粒体蛋白质组进行分析和鉴定。使用Blast2GO程序针对非冗余蛋白质数据库、京都基因与基因组百科全书数据库和直系同源蛋白质簇数据库对鉴定出的蛋白质进行分类和分组。与对照组相比,HFD组的mtDNA拷贝数、MMP以及MRC I和III的活性显著降低。共鉴定出18种上调蛋白和13种下调蛋白,对照组和NASH组之间存在显著的1.2倍差异。失调的蛋白质与线粒体氧化磷酸化、脂质代谢过程和脂肪酸β氧化密切相关。本研究结果提供了有关NASH肝线粒体的重要蛋白质组学信息,并为进一步详细研究NASH的发病机制奠定了基础。