Neuroprotective effect of mogrol against Aβ1-42-induced memory impairment neuroinflammation and apoptosis in mice

Objectives Cognitive impairment is the main character of Alzheimer's disease (AD). This study mainly focused on whether mogrol, a tetracyclic triterpenoids compound of Siraitia grosvenorii Swingle, can ameliorate the memory impairment induced by A beta(1-42). Methods Memory impairment mice model was made by stereotactic intra-hippocampal microinjection of A beta(1-42) (410 pm/mouse). Mogrol (20, 40, 80 mg/kg) was given to mice by intragastric administration at 3 days after A beta(1-42) injection for totally 3 weeks. Morris water maze test and Y-maze test were operated to evaluate the therapeutic effect of morgrol on A beta(1-42)-induced memory impairments. Immunohistochemical analyses and Hoechst 33258 assay were used to evaluate effect of morgrol on A beta(1-42)-induced microglia overactivation and apoptotic response in hippocampus of mice. Western blotting assay was used to evaluate effect of mogrol on the A beta(1-42)-activated NF-kappa B signaling. Key findings Mogrol could significantly alleviate A beta(1-42)-induced memory impairments, inhibit A beta(1-42)-induced microglia overactivation and prevent A beta(1-42)-triggered apoptotic response in the hippocampus. Mogrol also could suppress A beta(1-42)-activated NF-kappa B signaling, reduce the production of proinflammatory cytokines. Conclusions This study suggested that mogrol would ameliorate the memory impairment induced by A beta(1-42), which is involved in anti-inflammation and anti-apoptosis in the brain.