论文部分内容阅读
目的 :探讨重组腺病毒感染小鼠肝脏后,对肝脏的能量代谢和氧化应激水平的影响。方法 :将Balb/c小鼠随机分为正常组及重组腺病毒感染组,通过小鼠尾静脉注射含编码绿色荧光蛋白(GFP)外源基因的重组腺病毒,利用荧光显微镜观察GFP在肝脏的表达水平;检测血浆中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、葡萄糖、胆固醇、甘油三酯、β-羟丁酸(β-HB)、成纤维细胞生长因子(FGF-21)、丙二醛(MDA)等水平;测定肝脏糖原含量;检测肝脏组织中参与糖异生、脂质合成、脂肪酸氧化等基因的表达水平。结果:重组腺病毒主要在小鼠肝脏表达,并于注射后第5天表达最高。与对照组小鼠比较,重组腺病毒感染小鼠的血浆中ALT、AST明显升高,β-HB和FGF-21呈升高趋势。Real-time PCR检测发现,重组腺病毒感染小鼠的肝脏组织中,参与糖异生及脂质合成的基因m RNA水平明显降低,而脂肪酸氧化相关基因的m RNA水平明显升高。此外,重组腺病毒感染后,小鼠血浆MDA及肝脏中氧自由基产生基因的表达水平明显增高。结论:小鼠肝脏在感染重组腺病毒后,糖异生及脂质合成能力下降,而脂肪酸氧化增强。这种能量代谢的改变可能与重组腺病毒感染引起的氧化应激有关。
Objective: To investigate the effects of recombinant adenovirus on the liver’s energy metabolism and oxidative stress in mice infected with adenovirus. Methods: Balb / c mice were randomly divided into normal group and recombinant adenovirus group. The recombinant adenovirus containing green fluorescent protein (GFP) gene was injected through the tail vein of mice. The expression of GFP in liver (ALT), aspartate aminotransferase (AST), glucose, cholesterol, triglyceride, β-hydroxybutyrate (β-HB), fibroblast growth (FGF-21) and malondialdehyde (MDA). The content of liver glycogen was measured. The expression of genes involved in gluconeogenesis, lipid synthesis and fatty acid oxidation were detected in liver tissues. Results: The recombinant adenovirus was mainly expressed in the liver of mice and was the highest on the 5th day after injection. Compared with the control group, ALT, AST, and β-HB and FGF-21 levels in the plasma of mice infected with recombinant adenovirus were significantly increased. Real-time PCR showed that m RNA levels in genes involved in gluconeogenesis and lipid synthesis were significantly decreased in liver tissues of mice infected with recombinant adenovirus, whereas m RNA levels in fatty acid oxidation-related genes were significantly increased. In addition, the expression levels of MDA and liver oxygen free radicals in mouse plasma were significantly increased after recombinant adenovirus infection. Conclusion: In mice infected with recombinant adenovirus, the ability of gluconeogenesis and lipid synthesis decreased, while fatty acid oxidation increased. This change in energy metabolism may be related to oxidative stress caused by recombinant adenovirus infection.