Neurodegenerative diseases are characterized by progressive and selective degeneration of neurons in specific functional systems of the central and/or peripheral nervous system. They represent a significant human, societal and economic burden, which is continually growing as the elderly population i...
Neurodegenerative diseases are characterized by progressive and selective degeneration of neurons in specific functional systems of the central and/or peripheral nervous system. They represent a significant human, societal and economic burden, which is continually growing as the elderly population increases worldwide. Therefore the development of natural drug, which could minimize side effects, is urgently needed for prevention and treatment of neurodegenerative disorders. In this context, DPPH radical scavenging activity and MTT cell viability assay were performed as preliminary experiments to screen out promising candidates. Out of 18 plant extracts, onion showed most potent activity and quercetin was isolated as an active principle. In this study, the neuronal cell protective effects of quercetin and its protection mechanisms on the programmed cell death induced by glutamate in cultured hippocampal neuronal cells (HT22) were investigated. Quercetin, a component of ethyl acetate (EtOAc) soluble fraction of onion, showed HT22 cell protective effect by reducing the intracellular ROS overproduction induced by glutamate. These effects were due to down-regulation of various apoptosis-associated biochemical markers. In detail, the activity of calpain, which is a Ca2+-dependent protease, was effectively reduced by quercetin treatment. Moreover, spectrin cleavage was inhibited by quercetin on glutamate-exposed HT22 cells. In addition, disturbance of mitochondrial membrane potential, activation of pro-apoptotic Bcl-2 family, and cytochrome c release occurred by glutamate-mediated oxidative stress were reduced. Quercetin also remarkably suppressed the activation of ERK and p38. This is the first report on the detailed mechanisms of neuronal cell protective effect of quercetin. Quercetin mainly exists as glycoside forms, such as quercetin 3,4'-diglucoside and quercetin 4'-glucoside in the edible part of onion. Quercetin glycosides have been showed lower bioavailability and bioactivity than those of quercetin, therefore, fermentation of onion might be an useful tool for bioconversion of quercetin glycosides into quercetin. The content of quercetin was increased by fermentation about 61 times. Our results explain how quercetin attenuates glutamate-induced neuronal cell death and suggest possible strategies for prevention and treatment of neurodegenerative diseases.
Neurodegenerative diseases are characterized by progressive and selective degeneration of neurons in specific functional systems of the central and/or peripheral nervous system. They represent a significant human, societal and economic burden, which is continually growing as the elderly population increases worldwide. Therefore the development of natural drug, which could minimize side effects, is urgently needed for prevention and treatment of neurodegenerative disorders. In this context, DPPH radical scavenging activity and MTT cell viability assay were performed as preliminary experiments to screen out promising candidates. Out of 18 plant extracts, onion showed most potent activity and quercetin was isolated as an active principle. In this study, the neuronal cell protective effects of quercetin and its protection mechanisms on the programmed cell death induced by glutamate in cultured hippocampal neuronal cells (HT22) were investigated. Quercetin, a component of ethyl acetate (EtOAc) soluble fraction of onion, showed HT22 cell protective effect by reducing the intracellular ROS overproduction induced by glutamate. These effects were due to down-regulation of various apoptosis-associated biochemical markers. In detail, the activity of calpain, which is a Ca2+-dependent protease, was effectively reduced by quercetin treatment. Moreover, spectrin cleavage was inhibited by quercetin on glutamate-exposed HT22 cells. In addition, disturbance of mitochondrial membrane potential, activation of pro-apoptotic Bcl-2 family, and cytochrome c release occurred by glutamate-mediated oxidative stress were reduced. Quercetin also remarkably suppressed the activation of ERK and p38. This is the first report on the detailed mechanisms of neuronal cell protective effect of quercetin. Quercetin mainly exists as glycoside forms, such as quercetin 3,4'-diglucoside and quercetin 4'-glucoside in the edible part of onion. Quercetin glycosides have been showed lower bioavailability and bioactivity than those of quercetin, therefore, fermentation of onion might be an useful tool for bioconversion of quercetin glycosides into quercetin. The content of quercetin was increased by fermentation about 61 times. Our results explain how quercetin attenuates glutamate-induced neuronal cell death and suggest possible strategies for prevention and treatment of neurodegenerative diseases.
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