Ethyl Acetate Extracts of Bushen-Yizhi Formula Attenuates Aging-Induced Dementia through Suppressing NLRP3 Inflammasome Activation in SAMP8 Mice

Research Square (Research Square)(2020)

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摘要
Abstract Background: Similar features indicated common regulators between aging and aging-induced dementia, which demonstrated profound correlations with each other. However, the mechanism remains unclear. Bushen-Yizhi Formula(BSYZ-F) has been used for managing dementia in the clinic for hundreds of years. In this study, we aimed to further explore the mechanism of athyl acetate extracts of BSYZ-F(BSYZ-E) attenuates aging-induced dementia in Senescence-Accelerated Mouse Prone 8 (SAMP8) mice.Methods: As an age-related model, SAMP8 mice have been assigned to receive the corresponding interventions in this study. The Morris water maze was used to evaluate the learning and memory ability in SAMP8 mice. The marker level of oxidative stress(ROS and SOD) and nitrosative stress(NO and iNOS) were measured using commercial kits. The quantification of inflammation-related proteins (NLRP3, ASC, Caspase-1, IL-1β, and IL-18) and related apoptotic proteins (Bax, Bcl-2, Caspase-3, and Cleaved-Caspase-3) in hippocampal tissue were measured using Western blot.Results: In behavioral, the Morris Water Maze test demonstrated BSYZ-E alleviated the cognitive impairments in SAMP8 mice. Mechanism studies indicated that BSYZ-E increased the vitality of SOD, declined the validity of NO, iNOS, and MDA in SAMP8 mice. Besides, BSYZ-E relieved neuronal apoptosis by regulating the expression of related apoptotic proteins (Bax, Bcl-2, Caspase-3, and Cleaved-Caspase-3) and inhibited NLRP3 inflammasome activation by inflammation-related proteins (NLRP3, ASC, Caspase-1, IL-1β, and IL-18) in SAMP8 mice. Conclusions: These results suggested that BSYZ-E attenuates aging-induced dementia by suppressing the activation of NLRP3 inflammasome in SAMP8 mice.
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nlrp3 inflammasome activation,dementia,bushen-yizhi,aging-induced
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