scholarly journals Indole-6-Carboxaldehyde Isolated from Sargassum thunbergii (Mertens) Kuntze Prevents Oxidative Stress-Induced Cellular Damage in V79-4 Chinese Hamster Lung Fibroblasts through the Activation of the Nrf2/HO-1 Signaling Pathway

2020 ◽  
Vol 54 (5) ◽  
pp. 959-974 ◽  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Chinese Hamster ◽  
Cellular Damage ◽  
Lung Fibroblasts ◽  
Sargassum Thunbergii

8. Evaluation of Snow Fungus Polysaccharides on benzo[a]pyrene-induced DNA Damage

2018 ◽  
Author(s):  
Daisy Liu
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Free Radical ◽  
Radical Scavenging ◽  
Chinese Hamster ◽  
Negative Control ◽  
Lung Fibroblasts ◽  
Protective Effects ◽  
Tremella Fuciformis

Snow fungus, Tremella fuciformis, has been demonstrated to have numerous health benefits including purported chemopreventive properties due to free radical-scavenging ability. Protective effects derived from snow fungus polysaccharides are evaluated on Chinese hamster lung fibroblasts (CCL-39) exposed to carcinogen benzo[a]pyrene known to cause free radical formation and oxidative stress to cells. In this experiment, it was hypothesized that the naturally occurring polysaccharides in snow fungus are able to protect against or reduce oxidative stress-induced DNA damage. Polysaccharides were isolated through an alkaline extraction and in-vitro digestion. DNA damage was measured using the single-cell gel electrophoresis comet assay after exposure to benzo[a]pyrene and polysaccharide extract to lung fibroblasts. Results were calculated using the mean and standard deviation data of tail length and area, respectively. Each damaged cell was measured and analyzed through ImageJ Editing Software. The results indicate a promising trend which depict snow fungus polysaccharides yielding lower levels of DNA damage compared to cells exposed to benzo[a]pyrene and compared to the negative control (phosphate buffered saline and Dulbecco’s cell medium). This study suggests polysaccharides from Tremella fuciformis could truly prevent cellular DNA damage by protecting against oxidative stress.

Dithiocarbamate fungicide zineb induces oxidative stress and apoptosis in Chinese hamster lung fibroblasts

2012 ◽  
Vol 102 (1) ◽  
pp. 95-101 ◽  
Author(s):  
Emilia Grosicka-Maciąg ◽  
Dagmara Kurpios-Piec ◽  
Maria Szumiło ◽  
Tomasz Grzela ◽  
Iwonna Rahden-Staroń
Keyword(s):  
Oxidative Stress ◽  
Chinese Hamster ◽  
Lung Fibroblasts

scholarly journals Photoprotective Effects of Sargassum Thunbergii on Ultraviolet B-Induced Mouse L929 Fibroblasts and Zebrafish

2021 ◽  
Author(s):  
Bei Chen ◽  
Honghong Chen ◽  
Haidong Qu ◽  
Kun Qiao ◽  
Min Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Inflammatory Cytokine ◽  
Dna Condensation ◽  
Ultraviolet B ◽  
Uvb Radiation ◽  
Sargassum Thunbergii ◽  
L929 Cells ◽  
Mda Content

Abstract Background: Chronic exposure to ultraviolet B (UVB) causes a series of adverse skin reactions, such as erythema, sunburn, photoaging, and cancer, by altering signaling pathways related to inflammation, oxidative stress, and DNA damage. Marine algae have abundant amounts and varieties of bioactive compounds that possess antioxidant and anti-inflammatory properties. Thus, the objective of this study was to investigate the photoprotective effects of an ethanol extract of Sargassum thunbergii.Methods: Sargassum thunbergii phenolic-rich extract (STPE) was prepared, and its activity against UVB damage was evaluated using L929 fibroblast cells and zebrafish. STPE was extracted and purified by 40% ethanol and macroporous resin XDA-7. Reactive oxygen species (ROS) and antioxidant markers, such as superoxide dismutase (SOD), catalase (CAT) activities, and malondialdehyde (MDA) content were analyzed. The effect of STPE on UVB-induced inflammation was determined by inflammatory cytokine gene and protein expression. The expression of signaling molecules in the Nuclear Factor KappaB (NF-κB) pathway was determined by western blotting. DNA condensation was analyzed and visualized by Hoechst 33342 staining. In vivo evaluation was performed by tail fin area and ROS measurement using the zebrafish model. Results: The total polyphenol content of STPE was 72%. STPE reduced ROS content in L929 cells, improved SOD and CAT activities, and significantly reduced MDA content, thereby effectively alleviating UVB radiation-induced oxidative damage. STPE inhibited the mRNA and protein expression of TNF-α, IL-6, and IL-1α. STPE reversed DNA condensation at concentrations of 20 and 40 μg/mL compared with the UVB control. Moreover, STPE inhibited NF-κB signaling pathway activation and alleviated DNA agglutination in L929 cells after UVB irradiation. Additionally, 1.67 μg/mL STPE significantly increased the tail fin area in zebrafish, and 0.8–1.6 μg/mL STPE effectively eliminated excessive ROS after UVB radiation. Conclusions: STPE inhibited UVB-induced oxidative stress, inflammatory cytokine expression, and DNA condensation via downregulation of the NF-κB signaling pathway, suggesting that it prevents UVB-induced cell damage and photoaging, and has potential for clinical development for skin disease treatment.

scholarly journals The role of Nrf2 in oxidative stress-induced endothelial injuries

2015 ◽  
Vol 225 (3) ◽  
pp. R83-R99 ◽  
Author(s):  
Bo Chen ◽  
Yanrong Lu ◽  
Younan Chen ◽  
Jingqiu Cheng
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Signaling Pathway ◽  
Target Genes ◽  
Initial Step ◽  
Cellular Damage ◽  
Related Factor ◽  
Antioxidant Genes ◽  
Failure To Protect

Endothelial dysfunction is an important risk factor for cardiovascular disease, and it represents the initial step in the pathogenesis of atherosclerosis. Failure to protect against oxidative stress-induced cellular damage accounts for endothelial dysfunction in the majority of pathophysiological conditions. Numerous antioxidant pathways are involved in cellular redox homeostasis, among which the nuclear factor-E2-related factor 2 (Nrf2)/Kelch-like ECH-associated protein 1 (Keap1)–antioxidant response element (ARE) signaling pathway is perhaps the most prominent. Nrf2, a transcription factor with a high sensitivity to oxidative stress, binds to AREs in the nucleus and promotes the transcription of a wide variety of antioxidant genes. Nrf2 is located in the cytoskeleton, adjacent to Keap1. Keap1 acts as an adapter for cullin 3/ring-box 1-mediated ubiquitination and degradation of Nrf2, which decreases the activity of Nrf2 under physiological conditions. Oxidative stress causes Nrf2 to dissociate from Keap1 and to subsequently translocate into the nucleus, which results in its binding to ARE and the transcription of downstream target genes. Experimental evidence has established that Nrf2-driven free radical detoxification pathways are important endogenous homeostatic mechanisms that are associated with vasoprotection in the setting of aging, atherosclerosis, hypertension, ischemia, and cardiovascular diseases. The aim of the present review is to briefly summarize the mechanisms that regulate the Nrf2/Keap1–ARE signaling pathway and the latest advances in understanding how Nrf2 protects against oxidative stress-induced endothelial injuries. Further studies regarding the precise mechanisms by which Nrf2-regulated endothelial protection occurs are necessary for determining whether Nrf2 can serve as a therapeutic target in the treatment of cardiovascular diseases.

scholarly journals Dihydrocaffeic Acid Prevents UVB-Induced Oxidative Stress Leading to the Inhibition of Apoptosis and MMP-1 Expression via p38 Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Mariana M. Oliveira ◽  
Bianca A. Ratti ◽  
Regina G. Daré ◽  
Sueli O. Silva ◽  
Maria da Conceição T. Truiti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Capacity ◽  
Signaling Pathway ◽  
Neutral Red ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Cellular Damage ◽  
Skin Damage ◽  
Mitochondria Membrane Potential ◽  
Neutral Red Assay

Chronic UVB exposure promotes oxidative stress, directly causes molecular damage, and induces aging-related signal transduction, leading to skin photoaging. Dihydrocaffeic acid (DHCA) is a phenolic compound with potential antioxidant capacity and is thus a promising compound for the prevention of UVB-induced skin photodamage. The aim of this study was to evaluate the antioxidant and protective effect of DHCA against oxidative stress, apoptosis, and matrix metalloproteinase (MMP) expression via the mitogen-activated protein kinase (MAPK) signaling pathway on L929 fibroblasts irradiated with UVB. DHCA exhibited high antioxidant capacity on 2,2-diphenyl-1-picrylhydrazyl (DPPH•), 2,2-azinobis-3-ethylbenzothiazoline-6-sulphonic acid (ABTS•+), and xanthine/luminol/xanthine oxidase (XOD) assays and reduced UVB-induced cell death in the neutral red assay. DHCA also modulated oxidative stress by decreasing intracellular reactive oxygen species (ROS) and extracellular hydrogen peroxide (H2O2) production, enhancing catalase (CAT) and superoxide dismutase (SOD) activities and reduced glutathione (GSH) levels. Hence, cellular damage was attenuated by DHCA, including lipid peroxidation, apoptosis/necrosis and its markers (loss of mitochondria membrane potential, DNA condensation, and cleaved caspase 9 expression), and MMP-1 expression. Furthermore, DHCA reduced the phosphorylation of MAPK p38. These findings suggest that DHCA can be used in the development of skin care products to prevent UVB-induced skin damage.

scholarly journals Lycopene alleviates oxidative stress via the PI3K/Akt/Nrf2pathway in a cell model of Alzheimer’s disease

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9308 ◽  
Author(s):  
Yinchao Fang ◽  
Shanshan Ou ◽  
Tong Wu ◽  
Lingqi Zhou ◽  
Hai Tang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signaling Pathway ◽  
Cell Model ◽  
Chinese Hamster ◽  
Antiapoptotic Proteins ◽  
Model Of Alzheimer’S Disease ◽  
Nrf2 Signaling Pathway ◽  
Underlying Mechanisms

Background & Aims Oxidative stress (OS) plays an important role in neurodegenerative diseases such as Alzheimer’s disease (AD). Lycopene is a pigment with potent antioxidant and anti-tumor effects. However, its potential role in central nervous system is not well-defined. The aim of this study was to investigate the effect of lycopene on the cell model of AD and determine its underlying mechanisms. Methods M146L cell is a double-transfected (human APP gene and presenlin-1 gene) Chinese hamster ovary (CHO) cell line that overexpresses β -amyloid (Aβ) and is an ideal cell model for AD. We treated cells with lycopene, and observed the effect of lycopene on M146L cells. Results Oxidative stress and apoptosis in M146L cells were significantly higher than those in CHO cells, suggesting that Aβ induced OS and apoptosis. Lycopene alleviated OS and apoptosis, activated the PI3K/Akt/Nrf2 signaling pathway, upregulated antioxidant and antiapoptotic proteins and downregulated proapoptotic proteins. Additionally, lycopene inhibited β -secretase (BACE) activity in M146L cells. These results suggest that lycopene inhibits BACE activity and protects M146L cells from oxidative stress and apoptosis by activating the PI3K/Akt/Nrf2 pathway. Conclusion Lycopene possibly prevents Aβ-induced damage by activating the PI3K/Akt/Nrf2 signaling pathway and reducing the expression of BACE in M146L cells.

Sign in / Sign up

Export Citation Format

Share Document