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。
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.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2000年第3期172-173,共2页
Chinese Journal of Gerontology
关键词
松果体
半乳糖
衰老模型
自由基
褪黑素
Pineal gland Galactose Aging model Free radical Melatonin