scholarly journals Protection of Iron-Induced Oxidative Damage in Neuroblastoma (SH-SY5Y) Cells by Combination of 1-(N-Acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one and Green Tea Extract

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Nittaya Chansiw ◽  
Kanokwan Kulprachakarn ◽  
Narisara Paradee ◽  
Adchara Prommaban ◽  
Somdet Srichairatanakool
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Green Tea ◽  
Cell Damage ◽  
Neuroblastoma Cells ◽  
Green Tea Extract ◽  
Mitochondrial Activity ◽  
Acetoxymethyl Ester ◽  
Labile Iron Pool ◽  
Tea Extract

Iron is a crucial trace element and essential for many cellular processes; however, excessive iron accumulation can induce oxidative stress and cell damage. Neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease, have been associated with altered iron homoeostasis causing altered iron distribution and accumulation in brain tissue. This study aims to investigate the protective effect of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) in combination with green tea extract (GTE) on iron-induced oxidative stress in neuroblastoma (SH-SY5Y) cells. Cells were cultured in medium with or without ferric chloride loading. Their viability and mitochondrial activity were assessed using MTT and JC-1 staining methods. Levels of the cellular labile iron pool (LIP), reactive oxygen species (ROS), and lipid-peroxidation products were determined using calcein acetoxymethyl ester, 2′,7′-dichlorohydrofluorescein diacetate, and TBARS-based assays, respectively. The viability of iron-loaded cells was found to be significantly increased after treatment with CM1 (10 µM) for 24 h. CM1 co-treatment with GTE resulted in a greater protective effect than their monotherapy. Combination of CM1 and GTE also reduced mitochondrial disruption and LIP content and ROS and TBARS production. In conclusion, the combination of CM1 and GTE exhibits protection against iron-induced oxidative stress in neuroblastoma cells.

scholarly journals Green tea extract and epigallocatechin 3-gallate reduced labile iron pool and protected oxidative stress in iron-loaded cultured hepatocytes

2012 ◽  
Vol 03 (08) ◽  
pp. 1140-1150 ◽  
Author(s):  
Somdet Srichairatanakool ◽  
Kanokwan Kulprachakarn ◽  
Kanjana Pangjit ◽  
Kovit Pattanapanyasat ◽  
Suthat Fuchaeron
Keyword(s):  
Oxidative Stress ◽  
Green Tea ◽  
Green Tea Extract ◽  
Cultured Hepatocytes ◽  
Labile Iron Pool ◽  
Labile Iron ◽  
Iron Pool ◽  
Tea Extract

Protective effect of green tea extract against proline-induced oxidative damage in the rat kidney

2016 ◽  
Vol 83 ◽  
pp. 1422-1427 ◽  
Author(s):  
Débora Delwing-Dal Magro ◽  
Roberto Roecker ◽  
Gustavo M. Junges ◽  
André F. Rodrigues ◽  
Daniela Delwing-de Lima ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protective Effect ◽  
Green Tea ◽  
Rat Kidney ◽  
Green Tea Extract ◽  
Tea Extract

scholarly journals Green Tea Extract Ameliorates Learning and Memory Deficits in Ischemic Rats via Its Active Component Polyphenol Epigallocatechin-3-gallate by Modulation of Oxidative Stress and Neuroinflammation

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Kuo-Jen Wu ◽  
Ming-Tsuen Hsieh ◽  
Chi-Rei Wu ◽  
W. Gibson Wood ◽  
Yuh-Fung Chen
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Learning And Memory ◽  
Green Tea ◽  
Memory Impairment ◽  
Memory Deficits ◽  
Green Tea Extract ◽  
Morris Water Maze Test ◽  
Learning And Memory Deficits ◽  
Tea Extract

Ischemic stroke results in brain damage and behavioral deficits including memory impairment. Protective effects of green tea extract (GTex) and its major functional polyphenol (−)-epigallocatechin gallate (EGCG) on memory were examined in cerebral ischemic rats. GTex and EGCG were administered 1 hr before middle cerebral artery ligation in rats. GTex, EGCG, and pentoxifylline (PTX) significantly improved ishemic-induced memory impairment in a Morris water maze test. Malondialdehyde (MDA) levels, glutathione (GSH), and superoxide dismutase (SOD) activity in the cerebral cortex and hippocampus were increased by long-term treatment with GTex and EGCG. Both compounds were also associated with reduced cerebral infraction breakdown of MDA and GSH in the hippocampus. Inin vitroexperiments, EGCG had anti-inflammatory effects in BV-2 microglia cells. EGCG inhibited lipopolysaccharide- (LPS-) induced nitric oxide production and reduced cyclooxygenase-2 and inducible nitric oxide synthase expression in BV-2 cells. GTex and its active polyphenol EGCG improved learning and memory deficits in a cerebral ischemia animal model and such protection may be due to the reduction of oxidative stress and neuroinflammation.

scholarly journals Green Tea Potentially Ameliorates Bisphenol A-Induced Oxidative Stress: AnIn VitroandIn SilicoStudy

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Hiral Suthar ◽  
R. J. Verma ◽  
Saumya Patel ◽  
Y. T. Jasrai
Keyword(s):  
Oxidative Stress ◽  
Bisphenol A ◽  
Green Tea ◽  
Binding Capacity ◽  
Venous Blood ◽  
Green Tea Extract ◽  
High Dose ◽  
Healthy Human ◽  
Tea Extract ◽  
Dose Dependent

The present investigation was an attempt to elucidate oxidative stress induced by bisphenol A on erythrocytes and its amelioration by green tea extract. For this, venous blood samples from healthy human adults were collected in EDTA vials and used for preparation of erythrocytes suspension. When erythrocyte suspensions were treated with different concentrations of BPA/H2O2, a dose-dependent increase in hemolysis occurred. Similarly, when erythrocytes suspensions were treated with either different concentrations ofH2O2(0.05–0.25 mM) along with BPA (50 μg/mL) or 0.05 mMH2O2along with different concentrations of BPA (50–250 μg/mL), dose-dependent significant increase in hemolysis occurred. The effect of BPA andH2O2was found to be additive. For the confirmation, binding capacity of bisphenol A with erythrocyte proteins (hemoglobin, catalase, and glutathione peroxidase) was inspected using molecular docking tool, which showed presence of various hydrogen bonds of BPA with the proteins. The present data clearly indicates that BPA causes oxidative stress in a similar way asH2O2. Concurrent addition of different concentrations (10–50 μg/mL) of green tea extract to reaction mixture containing high dose of bisphenol A (250 μg/mL) caused concentration-dependent amelioration in bisphenol A-induced hemolysis. The effect was significant (P<0.05). It is concluded that BPA-induced oxidative stress could be significantly mitigated by green tea extract.

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