Neuroprotective effects of 2,3,5,4′-tetrahydoxystilbene-2-O-β-D-glucoside from Polygonum multiflorum against glutamate-induced oxidative toxicity in HT22 cells

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• 作者：Sun Young Lee^a ; ¹ ; Sung Min Ahn^a ; ¹ ; Ziyu Wang^b ; Young Whan Choi^b ; Hwa Kyoung Shin^a ; ^c ; ^d ; Byung Tae Choi^a ; ^c ; ^d ; ^{choibt@pusan.ac.kr}
• 关键词：Polygonum multiflorum ; 2 ; 3 ; 5 ; 4&prime ; -tetrahydoxystilbene-2-O-β-D-glucoside ; Oxidative stress ; Mitochondrial dysfunction ; Neuroprotection
• 刊名：Journal of Ethnopharmacology
• 出版年：2017
• 出版时间：4 January 2017
• 年：2017
• 卷：195
• 期：Complete
• 页码：64-70
• 全文大小：979 K
• 卷排序：195

文摘

Since ancient times, Polygonum multiflorum Thunb. has been used to treat premature grey hair, dizziness, and blurred vision in East Asia. A major bioactive constituent of this medicinal herb, 2,3,5,4'-tetrahydoxystilbene-2-O-β-D-glucoside (THSG), has antioxidant activity and exerts beneficial effects on cognition and memory.Aim of the studyThe purpose of the current study was to determine if THSG affects hippocampal neuronal cell death and mitochondrial function following exposure to oxidative stress.Materials and methodsHT22 hippocampal cells with or without THSG pretreatment were exposed to glutamate, and the effects on cell viability and expression of molecules related to apoptotic cell death were examined using biochemical techniques, flow cytometry, western immunoblotting, and real-time polymerase chain reaction.ResultsPretreatment with THSG significantly attenuated glutamate-induced loss of cell viability and release of lactate dehydrogenase as well as apoptotic cell death. THSG inhibited generation of reactive oxygen species (ROS), expression of heme oxygenase-1, and activation of caspase-3 and calpain-1 proteases, all of which were increased by glutamate. THSG inhibited glutamate-induced disruption of mitochondrial membrane potential (MMP) and voltage-dependent anion channel-1. It also regulated the ratio of Bax to Bcl-2.ConclusionsThese results indicate that THSG has a marked neuroprotective effect against glutamate-induced hippocampal damage by decreasing ROS production and stabilizing MMP. These findings suggest the potential of THSG as a new therapeutic agent for the treatment of cognitive disorders.