Objectives： The aim of the study is to evaluate the cognitive-enhancing effects of hydrolysate of polyga- lasaponin （HPS） on senescence accelerate mouse P8 （SAMP8） mice, an effective Alzheimer＇s disease （AD） m...Objectives： The aim of the study is to evaluate the cognitive-enhancing effects of hydrolysate of polyga- lasaponin （HPS） on senescence accelerate mouse P8 （SAMP8） mice, an effective Alzheimer＇s disease （AD） model, and to research the relevant mechanisms. Methods： The cognitive-enhancing effects of HPS on SAMP8 mice were assessed using Morris water maze （MWM） and step-through passive avoidance tests. Then N-methyl-D-aspartate （NMDA） receptor subunit expression for both the cortex and hippocampus of mice was observed using Western blot- ting. Results： HPS （25 and 50 mg/kg） improved the escape rate and decreased the escape latency and time spent in the target quadrant for the SAMP8 mice in the MWM after oral administration of HPS for 10 d. Moreover, it decreased error times in the passive avoidance tests. Western blotting showed that HPS was able to reverse the levels of NMDAR1 and NMDAR2B expression in the cortex or hippocampus of model mice. Conclusions： The present study suggested that HPS can improve cognitive deficits in SAMP8 mice, and this mechanism might be associated with NMDA receptor （NMDAR）-related pathways.展开更多
基金Project supported by the Medicinal Science and Technology Research Project(No.BWS11J052)the Ministry of Science and Technology of China(No.2012ZX09J12201)the Department of Science and Technology of Xinjiang Uygur Autonomous Region,China(No.201491174)
文摘Objectives： The aim of the study is to evaluate the cognitive-enhancing effects of hydrolysate of polyga- lasaponin （HPS） on senescence accelerate mouse P8 （SAMP8） mice, an effective Alzheimer＇s disease （AD） model, and to research the relevant mechanisms. Methods： The cognitive-enhancing effects of HPS on SAMP8 mice were assessed using Morris water maze （MWM） and step-through passive avoidance tests. Then N-methyl-D-aspartate （NMDA） receptor subunit expression for both the cortex and hippocampus of mice was observed using Western blot- ting. Results： HPS （25 and 50 mg/kg） improved the escape rate and decreased the escape latency and time spent in the target quadrant for the SAMP8 mice in the MWM after oral administration of HPS for 10 d. Moreover, it decreased error times in the passive avoidance tests. Western blotting showed that HPS was able to reverse the levels of NMDAR1 and NMDAR2B expression in the cortex or hippocampus of model mice. Conclusions： The present study suggested that HPS can improve cognitive deficits in SAMP8 mice, and this mechanism might be associated with NMDA receptor （NMDAR）-related pathways.
