6-苄胺基嘌呤对D-半乳糖致小鼠脑组织氧化损伤的保护作用

Protective effects of 6-benzylaminopurine against oxidative damage in brain tissue of mice induced by D-galactose

目的观察6-苄氨基嘌呤(6-BA)对小鼠脑组织氧化损伤的保护作用。方法小鼠随机分为4组,对照组、模型组和低、高2个剂量实验组(6-BA,20,40 mg·kg-1),用D-半乳糖复制小鼠脑组织氧化损伤模型,连续给药6周。用分光光度法检测小鼠脑组织总超氧化物歧化酶(T-SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力和丙二醛(MDA)含量;HE染色观察形态结构,单细胞凝胶电泳观察DNA氧化损伤水平。结果与模型组相比,实验组小鼠的T-SOD、GSH-Px活力显著提高,MDA含量显著降低;同时,6-BA明显改善D-半乳糖诱发的形态损伤和DNA损伤。结论 6-BA对小鼠脑组织氧化损伤具有一定的保护作用。

Objective To study the protective effects of 6-benzylaminopurine（ 6-BA） on oxidative injury in mice brain induced by D-galactose（ D-gal）. Methods The mice were randomly divided into four groups,and named control group,model group,low dose experimental group,and high dose experimental group. Brain injury model was induced by D-gal. Mice in experimental group were administrated by 6-BA（ 20,40 mg·kg-1） by gavage once daily for 6 weeks. The activities of total-superoxide dismutase（ T-SOD）, glutathione peroxidase（ GSH-Px）,and the content of malondialdehyde（ MDA） were detected by spectrophotometer. Histological features of mice brain were observed by HE staining and DNA oxidative damage was measured by single cell gel electrophoresis. Results Compared with model group,treatment of6-BA inhibited significantly MDA generation and increased the activities of T-SOD and GSH-Px,and improve significantly morphology and DNA damage induced by D-gal. Conclusion 6-BA has protective effects against oxidative damage in brain tissue of mice induced by D-gal.