【摘要】 目的　探讨褪斑黑素清除自由基及抗氧化性。方法用Ｄ－半乳糖诱导昆明种小鼠形成衰老模型，同时给予模型外源性褪 黑素（ＭＴ），检测小鼠肝组织ＳＯＤ活性、肝及脑组织ＧＳＨ－Ｐｘ活性和ＭＤＡ含量、心脏组织ＬＰＦ水平的变化。结果模型小鼠肝组织 ＳＯＤ活性下降（Ｐ＜０．０５）：肝及脑组织ＧＳＨ－Ｐｘ活力降低（分别为Ｐ＜０．０５；Ｐ＜０，０１）、ＭＤＡ含量升高（分别为Ｐ＜０．０１；Ｐ＜０．０１），心 脏组织中ＬＰＦ水平增高（Ｐ＜０． ０１）。给予外源性ＭＴ（５ ｍｇ／ｋｇ· ｄ－１）能明显提高ＧＳＨ－Ｐｘ活力（Ｐ＜０， ０１），降低组织ＭＤＡ及ＬＰＦ含量 （分别为 Ｐ＜０． ０１：Ｐ＜０． ０１）。而ＭＴ（１０ μｇ／ｋｘ· ｄ－１）除能提高模型动物体内组织ＧＳＨ－Ｐｘ活力外（Ｐ＜０． ０１），对其它指标作用不明显。 结论药物剂量的 ＭＴ（５ ｍｇ／ｋｇ）能明显阻止由Ｄ－半乳糖所致的小鼠体内的损伤变化，这主要是由于 ＭＴ清除自由基及激活抗氧化酶 作用，而生理剂量的ＭＴ作用有限。更多还原

【Abstract】 Objective Superoxide dismutase (SOD) activity of liver, glutathione peroxidase (GSH-Px) activities and molondialdehyde (MDA) levels in liver and brain,the content of lipofuscin(LPF) in heart were measured after intraperitoneal administration of melatonin to the D-galactose induced aging mice model. Results SOD and GSH-Px,activities were decreased in tissues of aging models,with MDA and LPF contents were increased. While the group treated with melatonin(ip 5 mg/kg·d-1) showed that GSH- Px activities were higher (P<0. 01),the amount of MDA and LPF were lower. While melatonin(ip 10 μg/kg·d-1 ) failed to prevent the lipid perosidation except for stimulating GSH-Px activities. Conclusions D-galactose can induce mimetic aging changes in mice, The pharmacological level of melatonin(5 mg/kg·d-1) remarkably counteracts the destructive actions induced by D-galactose. The results dues to scavenging free radicals directly and stimulating the antioxidant enzyme by melatonin.更多还原