Abstract：Objective To explore the neuroprotective effect of sulforaphane in mice with Alzheimer’s disease (AD)-like lesions so as to provide a theoretical basis for prevention and treatment of AD. Methods Thirty healthy male adult C57BL/6J mice were randomly divided into 3 groups based on their body weight, a control group, a model group and an intervention group, with 10 mice in each group. Mice in the model group and intervention group drank water containing aluminum (0.4 g/100 ml) ad libitum daily and were subcutaneously injected with D-galactose (200 mg/kg body weight) every other day, while the mice in the control group drank distilled water and received a subcutaneous injection of an equivalent amount of physiological saline instead. Besides, the mice in the intervention group were gavaged with 25 mg/kg SFN (perpared with distilled water) once a day, whereas the mice in the control group and the model group were gavaged with an equivalent amount of distilled water. The mice were observed daily for general condition and weighed each week. After 90 days, their spatial cognitive ability was evalated by morris water maze test.Senile plaque(SP) deposits in the brain was detected by congo red staining.The expression of G proten β2 subunit(Gβ2) mRNA and intracellular calcium level in the cerebral cortex were examined by real-time PCR assay and flow cytometry respectively. Results During the experiment, neither significant sign of toxicity nor death was observed in mice, and no statistically significant difference was found in the body weight of the mice among the three groups (P>0.05). Compared to the control group, the mice in the model group had a significantly decreased cognitive ability (P<0.05) and remarkablely increased SP (P<0.01) in both hippocampus and cerebral cortex, as well as attenuated Gβ2 mRNA expression and elevated intracellular calcium in the cerebral cortex (P<0.05). Compared with the model group, SFN could remarkably improve the mice’s cognitive impairment (P<0.05), significantly decrease the number of SP in both hippocampus and cortex of the brain (P<0.01), upregulate Gβ2 mRNA expression (P<0.05) and attenuate intracellular calcium in the cerebral cortex. Conclusions SFN can obviously protect the brain from SP deposits and ameliorate cognitive deficits in mice with AD-like lesions, and its mechanism may be associated with SFN-induced up-regulation of G-protein level and protection against intracellular calcium overload.
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2016, Vol. 23 
