Cytocompatible cerium oxide-mediated antioxidative stress in inhibiting ocular inflammation-associated corneal neovascularization

With the fast development of nanotechnology, the nanomaterials start to cause people’s attention for potential toxic effect. In this paper, the cytotoxicity and oxidative stress caused by 20-nm cerium oxide (CeO2) nanoparticles in cultured human lung cancer cells was investigated. The sulforhodamine B method was employed to assess cell viability after exposure to 3.5, 10.5, and 23.3 μg/ml of CeO2 nanoparticles for 24, 48, and 72 h. Cell viability decreased significantly as a function of nanoparticle dose and exposure time. Indicators of oxidative stress and cytotoxicity, including total reactive oxygen species, glutathione, malondialdehyde, α-tocopherol, and lactate dehydrogenase, were quantitatively assessed. It is concluded from the results that free radicals generated by exposure to 3.5 to 23.3 μg/ml CeO2 nanoparticles produce significant oxidative stress in the cells, as reflected by reduced glutathione and α-tocopherol levels; the toxic effects of CeO2 nanoparticles are dose dependent and time dependent; elevated oxidative stress increases the production of malondialdehyde and lactate dehydrogenase, which are indicators of lipid peroxidation and cell membrane damage, respectively.

Download Full-text

In Vitro and In Vivo Antioxidant Activity of the New Magnetic-Cerium Oxide Nanoconjugates

Nanomaterials ◽

10.3390/nano9111565 ◽

2019 ◽

Vol 9 (11) ◽

pp. 1565 ◽

Cited By ~ 7

Author(s):

Turin-Moleavin ◽

Fifere ◽

Lungoci ◽

Rosca ◽

Coroaba ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Activity ◽

Iron Oxide ◽

Cerium Oxide ◽

Chemical Activation ◽

Radical Scavenging ◽

Cerium Oxide Nanoparticles ◽

Oxide Nanoparticles

Background. Cerium oxide nanoparticles present the mimetic activity of superoxide dismutase, being able to inactivate the excess of reactive oxygen species (ROS) correlated with a large number of pathologies, such as stents restenosis and the occurrence of genetic mutations that can cause cancer. This study presents the synthesis and biological characterisation of nanoconjugates based on nanoparticles of iron oxide interconnected with cerium oxide conjugates. Methods. The synthesis of magnetite-nanoceria nanoconjugates has been done in several stages, where the key to the process is the coating of nanoparticles with polyethyleneimine and its chemical activation-reticulation with glutaraldehyde. The nanoconjugates are characterised by several techniques, and the antioxidant activity was evaluated in vitro and in vivo. Results. Iron oxide nanoparticles interconnected with cerium oxide nanoparticles were obtained, having an average diameter of 8 nm. Nanoconjugates prove to possess superparamagnetic properties and the saturation magnetisation varies with the addition of diamagnetic components in the system, remaining within the limits of biomedical applications. In vitro free-radical scavenging properties of nanoceria are improved after the coating of nanoparticles with polyethylenimine and conjugation with magnetite nanoparticles. In vivo studies reveal increased antioxidant activity in all organs and fluids collected from mice, which demonstrates the ability of the nanoconjugates to reduce oxidative stress. Conclusion. Nanoconjugates possess magnetic properties, being able to scavenge free radicals, reducing the oxidative stress. The combination of the two properties mentioned above makes them excellent candidates for theranostic applications.

Download Full-text

An Immunohistochemical Study of the Increase in Antioxidant Capacity of Corneal Epithelial Cells by Molecular Hydrogen, Leading to the Suppression of Alkali-Induced Oxidative Stress

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/7435260 ◽

2020 ◽

Vol 2020 ◽

pp. 1-10

Author(s):

Cestmir Cejka ◽

Jan Kossl ◽

Vladimir Holan ◽

John H. Zhang ◽

Jitka Cejkova

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Antioxidant Capacity ◽

Molecular Hydrogen ◽

Reactive Oxygen ◽

Corneal Neovascularization ◽

Scar Formation ◽

Oxygen Species ◽

Buffer Solution ◽

Corneal Epithelial

Corneal alkali burns are potentially blinding injuries. Alkali induces oxidative stress in corneas followed by excessive corneal inflammation, neovascularization, and untransparent scar formation. Molecular hydrogen (H2), a potent reactive oxygen species (ROS) scavenger, suppresses oxidative stress and enables corneal healing when applied on the corneal surface. The purpose of this study was to examine whether the H2 pretreatment of healthy corneas evokes a protective effect against corneal alkali-induced oxidative stress. Rabbit eyes were pretreated with a H2 solution or buffer solution, by drops onto the ocular surface, and the corneas were then burned with 0.25 M NaOH. The results obtained with immunohistochemistry and pachymetry showed that in the corneas of H2-pretreated eyes, slight oxidative stress appeared followed by an increased expression of antioxidant enzymes. When these corneas were postburned with alkali, the alkali-induced oxidative stress was suppressed. This was in contrast to postburned buffer-pretreated corneas, where the oxidative stress was strong. These corneas healed with scar formation and neovascularization, whereas corneas of H2-pretreated eyes healed with restoration of transparency in the majority of cases. Corneal neovascularization was strongly suppressed. Our results suggest that the corneal alkali-induced oxidative stress was reduced via the increased antioxidant capacity of corneal cells against reactive oxygen species (ROS). It is further suggested that the ability of H2 to induce the increase in antioxidant cell capacity is important for eye protection against various diseases or external influences associated with ROS production.

Download Full-text

Cerium Oxide Nanoparticles Counteract the Oxidative Stress in Cardiac Progenitor Cells

NATO Science for Peace and Security Series A: Chemistry and Biology - Advanced Bioactive Compounds Countering the Effects of Radiological, Chemical and Biological Agents ◽

10.1007/978-94-007-6513-9_8 ◽

2013 ◽

pp. 101-112

Author(s):

Francesca Pagliari ◽

Paolo Di Nardo

Keyword(s):

Oxidative Stress ◽

Progenitor Cells ◽

Cerium Oxide ◽

Cerium Oxide Nanoparticles ◽

Oxide Nanoparticles ◽

Cardiac Progenitor Cells

Download Full-text

Cerium oxide nanoparticles protects against acrylamide induced toxicity in HepG2 cells through modulation of oxidative stress

Drug and Chemical Toxicology ◽

10.1080/01480545.2018.1477793 ◽

2018 ◽

Vol 42 (1) ◽

pp. 54-59 ◽

Cited By ~ 9

Author(s):

Aala Azari ◽

Mohammad Shokrzadeh ◽

Ehsan Zamani ◽

Nahid Amani ◽

Fatemeh Shaki

Keyword(s):

Oxidative Stress ◽

Cerium Oxide ◽

Hepg2 Cells ◽

Cerium Oxide Nanoparticles ◽

Oxide Nanoparticles

Download Full-text

Amarogentin from Gentiana rigescens Franch Exhibits Antiaging and Neuroprotective Effects through Antioxidative Stress

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/3184019 ◽

2020 ◽

Vol 2020 ◽

pp. 1-15

Author(s):

Dejene Disasa ◽

Lihong Cheng ◽

Majid Manzoor ◽

Qian Liu ◽

Ying Wang ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Antioxidant Activity ◽

Natural Products ◽

Survival Rate ◽

Pc12 Cells ◽

Neuroprotective Effects ◽

Replicative Lifespan ◽

Antioxidative Stress ◽

Gentiana Rigescens

In the present study, the replicative lifespan assay of yeast was used to guide the isolation of antiaging substance from Gentiana rigescens Franch, a traditional Chinese medicine. A compound with antiaging effect was isolated, and the chemical structure of this molecule as amarogentin was identified by spectral analysis and compared with the reported data. It significantly extended the replicative lifespan of K6001 yeast at doses of 1, 3, and 10 μM. Furthermore, amarogentin improved the survival rate of yeast under oxidative stress by increasing the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), and these enzymes’ gene expression. In addition, this compound did not extend the replicative lifespan of sod1, sod2, uth1, and skn7 mutants with K6001 background. These results suggested that amarogentin exhibited antiaging effect on yeast via increase of SOD2, CAT, GPx gene expression, enzyme activity, and antioxidative stress. Moreover, we evaluated antioxidant activity of this natural products using PC12 cell system, a useful model for studying the nervous system at the cellular level. Amarogentin significantly improved the survival rate of PC12 cells under H2O2-induced oxidative stress and increased the activities of SOD and SOD2, and gene expression of SOD2, CAT, GPx, Nrf2, and Bcl-x1. Meanwhile, the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) of PC12 cells were significantly reduced after treatment of the amarogentin. These results indicated that antioxidative stress play an important role for antiaging and neuroprotection of amarogentin. Interestingly, amarogentin exhibited neuritogenic activity in PC12 cells. Therefore, the natural products, amarogentin from G. rigescens with antioxidant activity could be a good candidate molecule to develop drug for treating neurodegenerative diseases.

Download Full-text

Aspirin Eugenol Ester Protects Vascular Endothelium From Oxidative Injury by the Apoptosis Signal Regulating Kinase-1 Pathway

Frontiers in Pharmacology ◽

10.3389/fphar.2020.588755 ◽

2020 ◽

Vol 11 ◽

Author(s):

Mei-Zhou Huang ◽

Zhen-Dong Zhang ◽

Ya-Jun Yang ◽

Xi-Wang Liu ◽

Zhe Qin ◽

...

Keyword(s):

Oxidative Stress ◽

Vascular Endothelium ◽

Cell Apoptosis ◽

Oxidative Injury ◽

Vital Role ◽

Stress Effect ◽

Antioxidative Stress ◽

Aspirin Eugenol Ester

Aspirin eugenol ester (AEE) is a new potential pharmaceutical compound possessing anti-inflammatory, anti-cardiovascular disease, and antioxidative stress activity. The pharmacological activities of AEE are partly dependent on its regulation of cell apoptosis. However, it is still unclear how AEE inhibits cell apoptosis on the basis of its antioxidative stress effect. This study aimed to reveal the vascular antioxidative mechanism of AEE in response to H2O2-induced oxidative stress in HUVECs and paraquat-induced oxidative stress in rats. In the different intervention groups of HUVECs and rats, the expression of ASK1, ERK1/2, SAPK/JNK, and p38 and the phosphorylation levels of ERK1/2, SAPK/JNK, and p38 were measured. The effects of ASK1 and ERK1/2 on the anti-apoptotic activity of AEE in the oxidative stress model were probed using the corresponding inhibitors ASK1 and ERK1/2. The results showed that in the HUVECs, 200 μM H2O2 treatment significantly increased the phosphorylation of SAPK/JNK and the level of ASK1 but decreased the phosphorylation of ERK1/2, while in the HUVECs pretreated with AEE, the H2O2-induced changes were significantly ameliorated. The findings were observed in vitro and in vivo. Moreover, inhibition of ASK1 and ERK1/2 showed that ASK1 plays a vital role in the protective effect of AEE on H2O2-induced apoptosis. All findings suggested that AEE protects the vascular endothelium from oxidative injury by mediating the ASK1 pathway.

Download Full-text