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应用PCR技术 ,检测小鼠心肌、骨骼肌、肝脏、肾脏和大脑等组织mtDNA的缺失 ,探讨衰老及有氧运动训练延缓衰老的可能机制。结果发现 ,老年小鼠各组织mtDNA 3 866bp片段缺失发生率高于青年鼠。在所测的五种组织中肝脏mtDNA的缺失比例最低 ,大脑最高 ,说明衰老线粒体的功能下降是多系统的 ,但程度表现不均衡。长期有氧运动训练可显著减少 3 866bp片段缺失在心肌及骨骼肌中的积累 ,但肾脏mtDNA片段缺失有增多趋势 ,提示运动训练可能通过提高机体心肌、骨骼肌抗氧化应激能力 ,降低自由基影响 ,进而保护mtDNA。
The mtDNA deletion in myocardium, skeletal muscle, liver, kidney and brain of mice was detected by PCR, and the possible mechanism of anti-aging and aerobic exercise training was explored. The results showed that the incidence of mtDNA 3 866 bp deletion in the aged mice was higher than that in the young mice. Among the five tissues tested, the percentage of liver mtDNA deletion was the lowest and the brain was the highest, indicating that the decline of senescence mitochondrial function was multi-system, but the degree was not balanced. Long-term aerobic exercise significantly reduced the accumulation of 3 866 bp fragments in myocardium and skeletal muscle, but there was an increasing tendency of deletion of mtDNA fragments in kidney, which indicated that exercise training could reduce free radicals by increasing the antioxidant capacity of myocardial and skeletal muscle Influence, and then protect mtDNA.