scholarly journals t-BHQ Protects Against Oxidative Damage and Maintains the Antioxidant Response in Malnourished Rats

Dose-Response ◽  
2018 ◽  
Vol 16 (3) ◽  
pp. 155932581879630 ◽  
Author(s):  
Graciela Gavia-García ◽  
María de los Ángeles Rosas-Trejo ◽  
Eduardo García-Mendoza ◽  
Rafael Toledo-Pérez ◽  
Mina Königsberg ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protective Effect ◽  
Antioxidant Response ◽  
Nuclear Factor Κb ◽  
Pharmacological Intervention ◽  
Antioxidant Enzyme Activities ◽  
Lactation Period ◽  
Oxidative Protein Damage ◽  
Lower Protein ◽  
Antioxidant Mechanisms

Objective: Tert-butylhydroquinone (t-BHQ) protective effect against oxidative damage in thymus from malnourished pops-rats was evaluated. Methods: Malnutrition in pops-rats was induced during the lactation period and first-, second-, and third-degree malnourished rats were studied (MN1, MN2, and MN3). To determine t-BHQ protective effect, lipid peroxidation (LPx) was assessed, as well as the carbonyl content. The reduced glutathione and glutathione disulfide content were determined and antioxidant enzyme activities were measured. Results: Oxidative protein damage, LPx, and Nuclear Factor-κB (NF-κB) content, increased in the MN2 and MN3 compared to well-nourished rats, associated with lower protein content and antioxidant activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase. Tert-butylhydroquinone treatment induced a protective effect against lipids and proteins oxidative damage, as well as decrease in NF-κB in MN rats and restored the antioxidant mechanisms, mostly GPx and SOD. No differences were found between male and female animals. Conclusions: Results show that higher body weight deficit leads to increased oxidative damage and probably inflammation, attributable to alterations in antioxidant mechanisms. These effects were reversed by the t-BHQ-treatment, which restores the antioxidant response. Our findings suggest that t-BHQ could be an interesting pharmacological intervention, but it needs to be studied further.

scholarly journals Insight into the Protective Effect of Salidroside against H2O2-Induced Injury in H9C2 Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Hui Gao ◽  
Xueping Liu ◽  
Kunming Tian ◽  
Yichong Meng ◽  
Cuicui Yu ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protective Effect ◽  
Underlying Mechanism ◽  
Antioxidant Enzyme Activities ◽  
H9c2 Cells ◽  
H2o2 Treatment ◽  
P53 Overexpression ◽  
Intracellular Ros ◽  
Wide Range ◽  
Related Proteins

Salidroside is the important active ingredient of Rhodiola species, which shows a wide range of pharmacological activities such as antioxidative stress, anti-inflammation, and antiliver fibrosis. In this paper, we aimed to study the protective effect and mechanism of salidroside against H2O2-induced oxidative damage in H9C2 cells by determining cell proliferation rate, intracellular reactive oxygen species (ROS) level, antioxidant enzyme activities, and the expression of apoptosis-related proteins. The results showed that salidroside significantly alleviated cell growth inhibition induced by H2O2 treatment in H9C2 cells, decreased the levels of intracellular ROS and malondialdehyde (MDA), and increased the activity of superoxide dismutase (SOD) and catalase (CAT); meanwhile, salidroside upregulated the expression of Bcl-2 while downregulated the expression of Bax, p53, and caspase-3 in H2O2-treated H9C2 cells. Furthermore, the antiapoptotic effect of salidroside was almost eliminated by the knockdown of Bcl-2. In the further exploration, the Bcl-2 expression was decreased by the p53 overexpression and increased by p53 knockdown in H2O2-treated H9C2 cells. Consequently, salidroside could protect H9C2 cells against H2O2-induced oxidative damage, and the underlying mechanism may be related to scavenging intracellular ROS, increasing the activities of intracellular antioxidant enzymes and inhibiting the expression of apoptosis-related proteins.

Protective effect of chitooligosaccharides on hydrogen peroxide-induced PC-12 cells death by inhibition of oxidative damage

2010 ◽  
Vol 34 (8) ◽  
pp. S27-S27
Author(s):  
Xueling Dai ◽  
Ping Chang ◽  
Ke Xu ◽  
Changjun Lin ◽  
Hanchang Huang ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Oxidative Damage ◽  
Protective Effect ◽  
Pc 12 Cells ◽  
Cells Death

Protective Effect of Chungkukjang from Sunchang Province against Cellular Oxidative Damage

2008 ◽  
Vol 13 (2) ◽  
pp. 90-94 ◽  
Author(s):  
Ji-Myung Choi ◽  
Na-Ri Yi ◽  
Kyoung-Chun Seo ◽  
Ji-Sook Han ◽  
Young-Ok Song ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protective Effect

scholarly journals Marine Compound 3-bromo-4,5-dihydroxybenzaldehyde Protects Skin Cells against Oxidative Damage via the Nrf2/HO-1 Pathway

Marine Drugs ◽  
2019 ◽  
Vol 17 (4) ◽  
pp. 234 ◽  
Author(s):  
Yea Seong Ryu ◽  
Pincha Devage Sameera Madushan Fernando ◽  
Kyoung Ah Kang ◽  
Mei Jing Piao ◽  
Ao Xuan Zhen ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Antioxidant Response ◽  
Signaling Cascades ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Skin Cells ◽  
Reverse Transcription Pcr ◽  
Extracellular Signal ◽  
Diphenyltetrazolium Bromide ◽  
Marine Compound

In this study, we aimed to illustrate the potential bio-effects of 3-bromo-4,5-dihydroxybenzaldehyde (3-BDB) on the antioxidant/cytoprotective enzyme heme oxygenase-1 (HO-1) in keratinocytes. The antioxidant effects of 3-BDB were examined via reverse transcription PCR, Western blotting, HO-1 activity assay, and immunocytochemistry. Chromatin immunoprecipitation analysis was performed to test for nuclear factor erythroid 2-related factor 2 (Nrf2) binding to the antioxidant response element of the HO-1 promoter. Furthermore, the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed that the cytoprotective effects of 3-BDB were mediated by the activation of extracellular signal-regulated kinase (ERK) and protein kinase B (PKB, Akt) signaling. Moreover, 3-BDB induced the phosphorylation of ERK and Akt, while inhibitors of ERK and Akt abrogated the 3-BDB-enhanced levels of HO-1 and Nrf2. Finally, 3-BDB protected cells from H2O2- and UVB-induced oxidative damage. This 3-BDB-mediated cytoprotection was suppressed by inhibitors of HO-1, ERK, and Akt. The present results indicate that 3-BDB activated Nrf2 signaling cascades in keratinocytes, which was mediated by ERK and Akt, upregulated HO-1, and induced cytoprotective effects against oxidative stress.

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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