Ho Shih-Ching, Liu Jue-Hao, Wu ReY-Yih
Traditional Chinese Medicine Division, Development Center for Biotechnology, 81 Chang Hsing Street, Taipei, Taiwan, ROC.
Biogerontology. 2003;4(1):15-8. doi: 10.1023/a:1022417102206.
We successfully established an oxidant damage of mimetic aging model using mice induced by D-galactose, and the mimetic aging model is relative to free radical and the accumulation of waste substances in metabolism. The animals were divided into 3 groups: (1) phosphate-buffered saline (PBS); (2) 1% D-galactose; (3) 5% D-galactose by subcutaneous injection every day. After 45 days, mice treated with D-galactose showed a significant increase in the malondialdehyde (MDA), total antioxidant status (TAS) and a decrease in superoxide dismutase (SOD) in the blood compared with the PBS group. In the brain, the D-galactose treated mice exhibited a higher level MDA and a lower level SOD activity. In the liver, only the 5% D-galactose group indicated a significant increase in MDA. By reference to the oxidative biomarkers in blood, brain and liver, we have confirmed the reliability of the mimetic aging model.
我们成功地利用D-半乳糖诱导的小鼠建立了氧化损伤模拟衰老模型,该模拟衰老模型与自由基及代谢废物的积累有关。将动物分为3组:(1)磷酸盐缓冲盐水(PBS);(2)1% D-半乳糖;(3)每天皮下注射5% D-半乳糖。45天后,与PBS组相比,用D-半乳糖处理的小鼠血液中的丙二醛(MDA)、总抗氧化状态(TAS)显著增加,超氧化物歧化酶(SOD)减少。在大脑中,用D-半乳糖处理的小鼠表现出较高水平的MDA和较低水平的SOD活性。在肝脏中,只有5% D-半乳糖组的MDA显著增加。通过参考血液、大脑和肝脏中的氧化生物标志物,我们证实了模拟衰老模型的可靠性。