Neuroprotective Effect of Quercetin against Damage Induced by Oxygen Deprivation in Cultured Rat Cortical Neurons.
- Author:
Hoon KIM
1
;
Jong Il PARK
;
Suk Woo LEE
;
Jung Soo PARK
Author Information
1. Department of Emergency Medicine and Medical Research Institute, College of Medicine, Chungbuk National University, Cheongjoo, Korea. nichekh2000@chungbuk.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Hypoxia;
Quercetin;
Antioxidants;
Cortical neurons
- MeSH:
Acetylcysteine;
Animals;
Anoxia;
Antioxidants;
Ascorbic Acid;
Asphyxia;
Biphenyl Compounds;
Brain Diseases, Metabolic;
Cell-Free System;
Enzyme-Linked Immunosorbent Assay;
Heart Arrest;
Neurons;
Neuroprotective Agents;
Oxygen;
Picrates;
Plants;
Quercetin;
Rats;
Reactive Oxygen Species;
Stroke
- From:Journal of the Korean Society of Emergency Medicine
2009;20(2):170-176
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Neuronal hypoxia is clinically related to stroke, cardiac arrest, asphyxia, and various cases involving metabolic encephalopathy, which has led to much research looking for new neuroprotective strategies. Quercetin belongs to an extensive class of polyphenolic flavonoid compounds, which are almost ubiquitous in plants and plant food sources. Quercetin is known as a strong free radical scavenger and an inhibitor of the production of reactive oxygen species (ROS). However, the effects of quercetin on hypoxia-induced oxidative cell damage have rarely been investigated. This report describes studies in cultured rat cortical neurons on the cellular effects of quercetin on neural damage induced by oxygen-deprivation. METHODS: The experiment was conducted in vitro using primary culture of rat cortical neurons. Hypoxia induction was performed with a hypoxic chamber. The free radical scavenging activity of quercetin was assayed in cell-free systems using a stable free radical, 1,1-diphenyl-2-picrylhydrazyl (DPPH). Cytotoxicity was studied with the MTT method. The optical density of the neurons was measured at 540 nm using an ELISA reader. We used an inverted microscope to examine the morphological changes that followed hypoxia induction and quercetin treatment. RESULTS: An anti-DPPH radical assay showed that quercetin inhibited the production of DPPH radicals in vitro and that its radical scavenging activity was superior to ascorbic acid and n-acetylcysteine. According to the MTT assay, incubation of cortical neurons with quercetin protected the neurons from hypoxia-induced cytotoxicity. CONCLUSIONS: The results of this study suggest that at a low concentration (100 nM) quercetin has a neuroprotective effect on hypoxia-induced neuronal cell death; at a high concentration (100 uM) the protective effects for hypoxiainduced neuronal damage were reduced because of quercetin's apoptotic effects.
