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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。
Objective To investigate the scavenging of free radicals and antioxidation by methopeimin. Methods D-galactose was used to induce senile model in Kunming mice. Exogenous melatonin (MT) was also given. The activity of liver SOD, the activity of GSH-Px and MDA in liver and brain tissue, and heart tissue were detected. Changes in LPF levels. Results SOD activity in the liver of model mice was decreased (P<0.05): GSH-Px activity in liver and brain tissues was decreased (P<0.05; P<0,01) and MDA content was increased (P respectively). <0.01; P <0.01), LPF levels in cardiac tissue increased (P <0. 01). Administration of exogenous MT (5 mg/kg·d-1) significantly increased GSH-Px activity (P<0,01) and decreased tissue MDA and LPF levels (P<0.01, P<0.01, respectively). ). However, MT (10 μg/kx·d-1) could not increase the GSH-Px activity in model animals (P<0.01), but had no effect on other indicators. Conclusion The drug dose of MT (5 mg/kg) can significantly prevent the damage caused by D-galactose in mice. This is mainly due to MT scavenging free radicals and activation of antioxidant enzymes, while the physiological dose of MT limited.