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

Abstract

Abstract 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 Aβ1–42. Methods Memory impairment mice model was made by stereotactic intra-hippocampal microinjection of Aβ1–42 (410 pm/mouse). Mogrol (20, 40, 80 mg/kg) was given to mice by intragastric administration at 3 days after Aβ1–42 injection for totally 3 weeks. Morris water maze test and Y-maze test were operated to evaluate the therapeutic effect of morgrol on Aβ1–42-induced memory impairments. Immunohistochemical analyses and Hoechst 33258 assay were used to evaluate effect of morgrol on Aβ1–42-induced microglia overactivation and apoptotic response in hippocampus of mice. Western blotting assay was used to evaluate effect of mogrol on the Aβ1–42-activated NF-κB signaling. Key findings Mogrol could significantly alleviate Aβ1–42-induced memory impairments, inhibit Aβ1–42-induced microglia overactivation and prevent Aβ1–42-triggered apoptotic response in the hippocampus. Mogrol also could suppress Aβ1–42-activated NF-κB signaling, reduce the production of proinflammatory cytokines. Conclusions This study suggested that mogrol would ameliorate the memory impairment induced by Aβ1–42, which is involved in anti-inflammation and anti-apoptosis in the brain.