scholarly journals Peer Review #2 of "Investigation into the effects of antioxidant-rich extract of Tamarindus indica leaf on antioxidant enzyme activities, oxidative stress and gene expression profiles in HepG2 cells (v0.1)"

2015 ◽  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Peer Review ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Hepg2 Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Antioxidant Enzyme Activities ◽  
Tamarindus Indica

scholarly journals Gene expression profiles in human HepG2 cells treated with extracts of the Tamarindus indica fruit pulp

2010 ◽  
Vol 5 (4) ◽  
pp. 331-341 ◽  
Author(s):  
Nurhanani Razali ◽  
Azlina A. Aziz ◽  
Sarni M. Junit
Keyword(s):  
Gene Expression ◽  
Hepg2 Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Fruit Pulp ◽  
Tamarindus Indica

scholarly journals Influence of Iron on Cytotoxicity and Gene Expression Profiles Induced by Arsenic in HepG2 Cells

2019 ◽  
Vol 16 (22) ◽  
pp. 4484
Author(s):  
Yonghua Wang ◽  
Yuxuan Liu ◽  
Su Liu ◽  
Bing Wu
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Hepg2 Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Interactive Effects ◽  
Lipid Peroxidation Product ◽  
Biological Processes ◽  
Mitochondrial Depolarization ◽  
Peroxidation Product

The toxicity of arsenic (As) could be influenced by many environmental factors and elements. Iron (Fe) is one of the elements that could be involved in As-induced toxicity. In this study, the interactive effects of Fe and As in HepG2 cells were analyzed based on cytotoxicity and transcriptomic analyses. The results showed that Fe could decrease cell viability and increase mitochondrial depolarization induced by As exposure. Oxidative stress and damage have been proven to be one of the main mechanisms of As toxicity. Our results showed that Fe increased the generation of reactive oxygen species (ROS) and lipid peroxidation product malondialdehyde (MDA) induced by As exposure. Microarray analysis further verified that Fe increased the alteration of gene expression and biological processes related to oxidative stress, cell proliferation, and the apoptotic signaling pathway caused by As exposure. Both results of cytotoxicity and transcriptomic analyses suggest that an increase of Fe in the human body could increase the As-induced toxicity, which should be considered during the health risk assessment of As.

scholarly journals Effects of glutamine supplementation on oxidative stress-related gene expression and antioxidant properties in rats with streptozotocin-induced type 2 diabetes

2011 ◽  
Vol 107 (8) ◽  
pp. 1112-1118 ◽  
Author(s):  
Pei-Hsuan Tsai ◽  
Jun-Jen Liu ◽  
Chui-Li Yeh ◽  
Wan-Chun Chiu ◽  
Sung-Ling Yeh
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Amino Acid ◽  
Oxidative Damage ◽  
Antioxidant Capacity ◽  
Enzyme Activities ◽  
Antioxidant Enzyme Activities ◽  
Related Gene ◽  
Gene Expressions ◽  
Oxidative Stress Related Gene

There are close links among hyperglycaemia, oxidative stress and diabetic complications. Glutamine (GLN) is an amino acid with immunomodulatory properties. The present study investigated the effect of dietary GLN on oxidative stress-relative gene expressions and tissue oxidative damage in diabetes. There were one normal control (NC) and two diabetic groups in the present study. Diabetes was induced by an intraperitoneal injection of nicotinamide followed by streptozotocin (STZ). Rats in the NC group were fed a regular chow diet. In the two diabetic groups, one group (diabetes mellitus, DM) was fed a common semi-purified diet while the other group received a diet in which part of the casein was replaced by GLN (DM-GLN). GLN provided 25 % of total amino acid N. The experimental groups were fed the respective diets for 8 weeks, and then the rats were killed for further analysis. The results showed that blood thioredoxin-interacting protein (Txnip) mRNA expression in the diabetic groups was higher than that in the NC group. Compared with the DM group, the DM-GLN group had lower glutamine fructose-6-phosphate transaminase 1, a receptor of advanced glycation end products, and Txnip gene expressions in blood mononuclear cells. The total antioxidant capacity was lower and antioxidant enzyme activities were altered by the diabetic condition. GLN supplementation increased antioxidant capacity and normalised antioxidant enzyme activities. Also, the renal nitrotyrosine level and Txnip mRNA expression were lower when GLN was administered. These results suggest that dietary GLN supplementation decreases oxidative stress-related gene expression, increases the antioxidant potential and may consequently attenuate renal oxidative damage in rats with STZ-induced diabetes.

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