Effects of sulforaphane on brain Aβ deposition and oxidative stress in Alzheimer's disease mice model
10.3760/cma.j.issn.0254-9026.2014.07.031
- VernacularTitle:莱菔硫烷对阿尔茨海默病小鼠脑组织Aβ沉积和氧化应激的影响
- Author:
Yue ZUO
;
Nan CHEN
;
Xi LI
;
Yue ZHAO
;
Li LIU
;
Li AN
- Publication Type:Journal Article
- Keywords:
Alzheimer's disease;
Sulforaphane;
Amyloid beta-protein;
Oxidative stress
- From:Chinese Journal of Geriatrics
2014;33(7):799-801
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the interventional effect of sulforaphane (SFN) on brain Aβ deposition and oxidative stress in Alzheimer's disease model mice.Methods Eight-week old C57BL/6J mice were randomly divided into three groups (n =10,each).Mice in two groups (intervention and model)were administered by drinking water containing 0.4g aluminum /100ml water and subcutaneous injection with 200mg/kg D-galactose every other day,added with 25mg/kg SFN to the intervention group or with equivalent double-distilled water to model group by a single oral gavage daily.And equivalent vehicle were given to the control mice.After 90 days,the aluminum levels in blood,brain Aβ depositions,and indices of oxidative stress in cerebral cortex were investigated.Results Blood aluminum level was higher in the AD model and SFN intervention groups than in controls(P＜0.01),and was lower in SFN intervention group than in AD model(P＜0.01).As compared to controls,the AD model showed that brain Aβ deposition was significantly increased,GPX activity was decreased and carbonyl level was remarkable increased(P＜0.05).There were no significant differences between intervention and control group in brain Aβ deposition,GPX activity and carbonyl contents (P＞0.05).Brain Aβ deposition was lower in intervention than in model group(P＜0.05).There was no significantly differences in brain SOD activity and total hydrosulfuryl content among three groups(P＞0.05).Conclusions Sulforaphane can reduce the aluminum level in blood,attenuate Aβ deposition,and regulate the oxidative stress in cerebral cortex in AD model mice.
