scholarly journals Protective effects of cannabidiol on the membrane proteins of skin keratinocytes exposed to hydrogen peroxide via participation in the proteostasis network

Redox Biology ◽  
2021 ◽  
pp. 102074
Author(s):  
Sinemyiz Atalay ◽  
Agnieszka Gęgotek ◽  
Pedro Domingues ◽  
Elżbieta Skrzydlewska
Keyword(s):  
Hydrogen Peroxide ◽  
Membrane Proteins ◽  
Protective Effects ◽  
Skin Keratinocytes

Protective efficacy of carnosic acid against hydrogen peroxide induced oxidative injury in HepG2 cells through the SIRT1 pathway

2015 ◽  
Vol 93 (8) ◽  
pp. 625-631 ◽  
Author(s):  
Yan Hu ◽  
Ning Zhang ◽  
Qing Fan ◽  
Musen Lin ◽  
Ce Zhang ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Hepg2 Cells ◽  
Manganese Superoxide Dismutase ◽  
Caspase 3 ◽  
Protective Efficacy ◽  
B Cell Lymphoma ◽  
Sirtuin 1 ◽  
Carnosic Acid ◽  
Protective Effects ◽  
Hepatocyte Damage

Carnosic acid (CA), found in rosemary, has been reported to have antioxidant and antiadipogenic properties. Here, we investigate the molecular mechanism by which CA inhibits hydrogen peroxide (H2O2)-induced injury in HepG2 cells. Cells were pretreated with 2.5–10 μmol/L CA for 2 h and then exposed to 3 mmol/L H2O2 for an additional 4 h. CA dose-dependently increased cell viability and decreased lactate dehydrogenase activities. Pretreatment with CA completely attenuated the inhibited expression of manganese superoxide dismutase (MnSOD) and the B-cell lymphoma-extra large (Bcl-xL), and reduced glutathione activity caused by H2O2, whereas it reversed reactive oxygen species accumulation and the increase in cleaved caspase-3. Importantly, sirtuin 1 (SIRT1), a NAD+-dependent deacetylase, was significantly increased by CA. Considering the above results, we hypothesized that SIRT1 may play important roles in the protective effects of CA in injury induced by H2O2. As expected, SIRT1 suppression by Ex527 (6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide) and siRNA-mediated SIRT1 silencing (si-SIRT1) significantly aggravated the H2O2-induced increased level of cleaved caspase-3 but greatly reduced the decreased expression of MnSOD and Bcl-xL. Furthermore, the positive regulatory effect of CA was inhibited by si-SIRT1. Collectively, the present study indicated that CA can alleviate H2O2-induced hepatocyte damage through the SIRT1 pathway.

Protective effects of ETC complex III and cytochromecagainst hydrogen peroxide-induced apoptosis in yeast

2014 ◽  
Vol 48 (4) ◽  
pp. 435-444 ◽  
Author(s):  
Chao-qun Wang ◽  
Xuan Li ◽  
Ming-qiang Wang ◽  
Jia Qian ◽  
Ke Zheng ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Complex Iii ◽  
Protective Effects ◽  
Induced Apoptosis

Anti-Apoptotic and Anti-Inflammatory Activities of Edible Fresh Water Algae Prasiola japonica in UVB-Irradiated Skin Keratinocytes

2019 ◽  
Vol 47 (08) ◽  
pp. 1853-1868
Author(s):  
Eunju Choi ◽  
Young-Su Yi ◽  
Jongsung Lee ◽  
Sang Hee Park ◽  
Sunggyu Kim ◽  
...  
Keyword(s):  
Fresh Water ◽  
Ethanol Extract ◽  
The Body ◽  
Hacat Cells ◽  
Protective Effects ◽  
Proteolytic Activation ◽  
Skin Keratinocytes ◽  
External Stresses ◽  
Anti Oxidant ◽  
Anti Inflammatory

Skin is the outer tissue layer and is a barrier protecting the body from various external stresses. The fresh water green edible algae Prasiola japonica has antiviral, antimicrobial, and anti-inflammatory properties; however, few studies of its effects on skin-protection have been reported. In this study, Prasiola japonica ethanol extract (Pj-EE) was prepared, and its skin-protective properties were investigated in skin keratinocytes. Pj-EE inhibited ROS production in UVB-irradiated HaCaT cells without cytotoxicity. Pj-EE also suppressed the apoptotic death of UVB-irradiated HaCaT cells by decreasing the generation of apoptotic bodies and the proteolytic activation of apoptosis caspase-3, -8, and -9. Moreover, Pj-EE downregulated the mRNA expression of the inflammatory gene cyclooxygenase-2 (COX-2), the pro-inflammatory cytokine genes interleukin (IL)-1[Formula: see text], IL-8, IL-6, tumor necrosis factor (TNF)-[Formula: see text], and interferon (IFN)-[Formula: see text], and the tissue remodeling genes matrix metalloproteinase (MMP)-1, -2, -3, and -9. The Pj-EE-induced anti-inflammatory effect was mediated by suppressing the activation of nuclear factor-kappa B (NF-[Formula: see text]B) signaling pathway in the UVB-irradiated HaCaT cells. Taken together, these results suggest that Pj-EE exerts skin-protective effects through anti-oxidant, anti-apoptotic, and anti-inflammatory activities in skin keratinocytes.

scholarly journals Total Glucosides of Peony Protect Cardiomyocytes against Oxidative Stress and Inflammation by Reversing Mitochondrial Dynamics and Bioenergetics

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Mengmeng Wang ◽  
Qiang Li ◽  
Ying Zhang ◽  
Hao Liu
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lupus Erythematosus ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Bioenergetics ◽  
Protective Effects ◽  
Systemic Lupus ◽  
Regulatory Effects ◽  
Total Glucosides Of Peony

Total glucosides of peony (TGP) are used to treat rheumatoid arthritis and systemic lupus erythematosus. We explored the protective effects of TGP on cardiomyocyte oxidative stress and inflammation in the presence of hydrogen peroxide by focusing on mitochondrial dynamics and bioenergetics. Our study demonstrated that hydrogen peroxide significantly repressed cardiomyocyte viability and promoted cell apoptosis through induction of the mitochondrial death pathway. TGP treatment sustained cardiomyocyte viability, reduced cardiomyocyte apoptosis, and decreased inflammation and oxidative stress. Molecular investigation indicated that hydrogen peroxide caused mitochondrial dynamics disruption and bioenergetics reduction in cardiomyocytes, but this alteration could be normalized by TGP. We found that disruption of mitochondrial dynamics abolished the regulatory effects of TGP on mitochondrial bioenergetics; TGP modulated mitochondrial dynamics through the AMP-activated protein kinase (AMPK) pathway; and inhibition of AMPK alleviated the protective effects of TGP on mitochondria. Our results showed that TGP treatment reduces cardiomyocyte oxidative stress and inflammation in the presence of hydrogen peroxide by correcting mitochondrial dynamics and enhancing mitochondrial bioenergetics. Additionally, the regulatory effects of TGP on mitochondrial function seem to be mediated through the AMPK pathway. These findings are promising for myocardial injury in patients with rheumatoid arthritis and systemic lupus erythematosus.

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