摘要
目的通过观察SOD1转基因小鼠骨骼肌中解偶联蛋白-3(UCP-3)表达水平的变化,探讨其在肌萎缩侧索硬化(ALS)疾病发生发展过程中的作用及意义。方法随机选取不同时期SOD1转基因模型雌性小鼠18只作为实验组,并选取非转基因同窝对照雌性小鼠18只为对照组,分别在生长不同阶段取两组小鼠骨骼肌为标本,应用Western blot及RT-PCR检测小鼠骨骼肌内UCP-3蛋白及其mRNA的表达水平变化,并对所得数据进行统计学分析。结果通过实验所得两组数据比较发现,实验组较对照组症状期、终末期UCP-3蛋白表达及mRNA表达均明显升高,且UCP-3蛋白表达与疾病发展呈时间相关趋势,差异有统计学意义(P<0.05)。结论本实验结果表明随着ALS疾病进展UCP-3蛋白及mRNA表达水平均明显升高,证实UCP-3可能通过参与机体抗氧化及代谢过程在ALS疾病发生发展中发挥重要作用。
Objective To observe the change of SOD1 transgenic mice skeletal muscle uncoupling protein 3( UCP-3),explore the role and significancein of UCP-3 amyotrophic lateral sclerosis( ALS).Methods Randomly selected from different periods transgenic male mice with the missense mutation( G93A) in the SOD1 mice as experimental group.Nontransgenic littermates served as controls.Each group includes eighteen mice. We used Western blot to detect the protein expression of UCP3 in all phases of transgenic mice and used RT-PCR to detect the mRNA expression of UCP3 in all phases of transgenic mice.The data were analyzed with SPSS 17.0.Results To compare the two groups,we found that the experimental group than the control group.onset,ending group UCP-3 protein expression and mRNA expression were significantly increased,and the UCP 3 protein expression and time related to the disease development trend,the differences were statistically significant( P < 0. 05). Conclusion The abnomal increase expression of UCP3 mRNA and protein expression in skeletal muscle of G93 A transgenic mice. It is confirmed that UCP3 can through anti-oxidation and participate in the body metabolic disorder in ALS disease.
出处
《脑与神经疾病杂志》
2014年第6期436-439,共4页
Journal of Brain and Nervous Diseases
基金
河北省科技厅科研基金项目(20100072)
关键词
肌萎缩侧索硬化
解偶联蛋-3
骨骼肌
转基因小鼠
Amyotrophic lateral sclerosis
Uncoupling protein 3
Skeletal muscle
SOD1-G93A transgenic mice