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《上海大学学报(自然科学版)》2019年25卷1期:001-009 小鼠非酒精性脂肪性肝炎中线粒体功能的障碍 Dysfunction of mitochondrial in mice with non-alcoholic steatohepatitis Abstract: [Objective] This research is to study the changes of mitochondrial function in non-alcoholic steatohepatitis (NASH).[Methods] The method is to use C57BL/6 mice fed with choline methionine deficient (MCD) diet to induce a mouse NASH model. The choline methionine sufficient (MCS) group serves as the control group. Four weeks later, serum and liver tissue are detected when mice are sacrificed. Biochemical indicators of serum alanine aminotransferase (ALT) activity, aspartate aminotransferase (AST) activity, liver triglyceride (TG), total cholesterol (TC) levels are detected by enzymelinked immunosorbent assay. Pathological examination has also been performed. The mtDNA/nDNA and nDNA in liver tissue of mice and the expression of genes encoded by mitochondrial DNA, mitochondrial DNA replication and associated with energy metabolism in mouse liver are tested by qRT-PCR (quantificational real-time polymerase chain reaction).[Results] Compared with the MCS group, the MCD model group shows severe degeneration of liver tissue, and ALT, AST, and TG become significantly elevated, but TC levels are decreased. A large amount of fat vacuoles, severe destruction of lobular structure, and significant infiltration of inflammatory cells become increased in MCD model. In addition, the amount of mitochondrial is decreased. Furthermore, the capacity of energy metabolism and DNA repair of the MCD model group are significantly reduced.[Conclusion] Mitochondrial dysfunction occurs in mice with non-alcoholic steatohepatitis. 全文链接:http://www.journal.shu.edu.cn/fileup/1007-2861/PDF/20190101.pdf |
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