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Article

Neuroprotective Effect of Gallocatechin Gallate on Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells

by 1,†, 2,†, 1,* and 1,*
1
College of Korean Medicine, Gachon University, Seongnam 13120, Korea
2
Department of Food Science and Biotechnology, Kyonggi University, Suwon 16227, Korea
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Angela Cardinali
Molecules 2021, 26(5), 1387; https://doi.org/10.3390/molecules26051387
Received: 28 January 2021 / Revised: 25 February 2021 / Accepted: 1 March 2021 / Published: 4 March 2021
(This article belongs to the Special Issue Antioxidant Activity of Food Constituents)
Oxidative stress leads to protein degeneration or mitochondrial dysfunction, causing neuronal cell death. Glutamate is a neurotransmitter that nerve cells use to send signals. However, the excess accumulation of glutamate can cause excitotoxicity in the central nervous system. In this study, we deciphered the molecular mechanism of catechin-mediated neuroprotective effect on glutamate-induced oxidative stress in mouse hippocampal neuronal HT22 cells. Cellular antioxidant activity was determined using the 1,1-diphenyl-picryl hydrazyl (DPPH) assay and 2′,7′-dichlorodihydrofluorescein diacetate (DCFDA) staining. Furthermore, the levels of intracellular calcium (Ca2+) as well as nuclear condensation and protein expression related to neuronal damage were assessed. All five catechins (epigallocatechin gallate, gallocatechin gallate (GCG), gallocatechin, epicatechin gallate, and epicatechin) showed strong antioxidant effects. Among them, GCG exhibited the highest neuroprotective effect against glutamate excitotoxicity and was used for further mechanistic studies. The glutamate-induced increase in intracellular Ca2+ was reduced after GCG treatment. Moreover, GCG reduced nuclear condensation and the phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinases (JNK) involved in cell death. The neuroprotective effect of GCG against glutamate-induced oxidative stress in HT22 cells was attributed to the reduction in intracellular free radicals and Ca2+ influx and also the inhibition of phosphorylation of ERK and JNK. Furthermore, the antioxidant effect of GCG was found to be likely due to the inhibition of phosphorylation of ERK and JNK that led to the effective suppression of neurocytotoxicity caused by glutamate in HT22 cells. View Full-Text
Keywords: gallocatechin gallate; ROS; HT22; Ca2+; antioxidant gallocatechin gallate; ROS; HT22; Ca2+; antioxidant
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MDPI and ACS Style

Park, D.H.; Park, J.Y.; Kang, K.S.; Hwang, G.S. Neuroprotective Effect of Gallocatechin Gallate on Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells. Molecules 2021, 26, 1387. https://doi.org/10.3390/molecules26051387

AMA Style

Park DH, Park JY, Kang KS, Hwang GS. Neuroprotective Effect of Gallocatechin Gallate on Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells. Molecules. 2021; 26(5):1387. https://doi.org/10.3390/molecules26051387

Chicago/Turabian Style

Park, Do H.; Park, Jun Y.; Kang, Ki S.; Hwang, Gwi S. 2021. "Neuroprotective Effect of Gallocatechin Gallate on Glutamate-Induced Oxidative Stress in Hippocampal HT22 Cells" Molecules 26, no. 5: 1387. https://doi.org/10.3390/molecules26051387

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