A new ocotillol-type ginsenoside from stems and leaves of Panax quinquefolium L. and its anti-oxidative effect on hydrogen peroxide exposed A549 cells

In recent years, the emergence of non-toxic but catalytically active inorganic nanoparticles has attracted great attention for cancer treatment, but the therapeutic effect has been affected by the limited reactive oxygen species in tumors. Therefore, the combination of chemotherapy and chemodynamic therapy is regarded as a promising therapeutic strategy. In this paper, we reported the preparation and bioactivity evaluation of poly(lactic acid-co-glycolic acid) (PLGA) grafted-γ-Fe2O3 nanoparticles with dual response of endogenous peroxidase and catalase like activities. Our hypothesis is that PLGAgrafted γ-Fe2O3 nanoparticles could be used as a drug delivery system for the anti-tumor drug doxorubicin to inhibit the growth of lung adenocarcinoma A549 cells; meanwhile, based on its mimic enzyme properties, this kind of nanoparticles could be combined with doxorubicin in the treatment of A549 cells. Our experimental results showed that the PLGAgrafted γ-Fe2O3 nanoparticles could simulate the activity of catalase and decompose hydrogen peroxide into H2O and oxygen in neutral tumor microenvironment, thus reducing the oxidative damage caused by hydrogenperoxide to lung adenocarcinoma A549 cells. In acidic microenvironment, PLGA grafted γ-Fe2O3 nanoparticles could simulate the activity of peroxidase and effectively catalyze the decomposition of hydrogen peroxide to generate highly toxic hydroxyl radicals, which could cause the death of A549 cells. Furthermore, the synergistic effect of peroxidase-like activity of PLGA-grafted γ-Fe2O3 nanoparticles and doxorubicin could accelerate the apoptosisand destruction of A549 cells, thus enhancing the antitumor effect of doxorubicin-loaded PLGA-grafted γ-Fe2O3 nanoparticles. Therefore, this study provides an effective nanoplatform based on dual inorganic biomimetic nanozymes for the treatment of lung cancer.

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A carbon-based nanocarrier for efficient gene delivery

Therapeutic Delivery ◽

10.4155/tde-2020-0135 ◽

2021 ◽

Author(s):

Tahereh Kashkoulinejad-Kouhi ◽

Shadi Sawalha ◽

Shahrokh Safarian ◽

Blanca Arnaiz

Keyword(s):

Hydrogen Peroxide ◽

Gene Delivery ◽

Water Solubility ◽

Chemotherapy Resistance ◽

A549 Cells ◽

Carbon Nanodots ◽

Simple Method ◽

Efficient Gene ◽

Low Toxicity ◽

Positively Charged

Aim: Several types of nanocarriers, most of which show significant cytotoxicity, have been developed to overcome the problem of gene-delivery barriers. Biocompatibility, low toxicity and water solubility of carbon nanodots (CNDs) are major advantages that recommend them as delivery systems. Materials & methods: We present a simple method to produce positively charged CNDs. Ethanolamine, ethylenediamine and hydrogen peroxide were utilized to synthesize these CNDs. Results & conclusion: Our results indicated that delivery of the CND–siGFP complex led to significant switching-off of the fluorescence of the GFP-expressing A549 cell. Next, the A549 cells were transfected with siRNA against BiP, which is a pivotal protein in the chemotherapy resistance of cancer cells. The expression levels of BiP decreased remarkably.

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Hydrogen peroxide-induced oxidative stress and its impact on innate immune responses in lung carcinoma A549 cells

Molecular and Cellular Biochemistry ◽

10.1007/s11010-018-3380-2 ◽

2018 ◽

Vol 450 (1-2) ◽

pp. 135-147 ◽

Cited By ~ 12

Author(s):

Shishir Upadhyay ◽

Saurabh Vaish ◽

Monisha Dhiman

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Immune Responses ◽

Lung Carcinoma ◽

A549 Cells ◽

Innate Immune ◽

Innate Immune Responses

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Hydrogen Sulfide Attenuates Hydrogen Peroxide-Induced Injury in Human Lung Epithelial A549 Cells

International Journal of Molecular Sciences ◽

10.3390/ijms20163975 ◽

2019 ◽

Vol 20 (16) ◽

pp. 3975 ◽

Cited By ~ 3

Author(s):

Mingqi Wang ◽

Xinyu Cao ◽

Chang Luan ◽

Zhengqiang Li

Keyword(s):

Hydrogen Peroxide ◽

Hydrogen Sulfide ◽

Lung Injury ◽

Er Stress ◽

Human Lung ◽

A549 Cells ◽

Mapk Signaling ◽

Protective Mechanism ◽

Lung Epithelial ◽

Pre Treatment

Lung tissues are frequently exposed to a hyperoxia environment, which leads to oxidative stress injuries. Hydrogen sulfide (H2S) is widely implicated in physiological and pathological processes and its antioxidant effect has attracted much attention. Therefore, in this study, we used hydrogen peroxide (H2O2) as an oxidative damage model to investigate the protective mechanism of H2S in lung injury. Cell death induced by H2O2 treatment could be significantly attenuated by the pre-treatment of H2S, resulting in a decrease in the Bax/Bcl-2 ratio and the inhibition of caspase-3 activity in human lung epithelial cell line A549 cells. Additionally, the results showed that H2S decreased reactive oxygen species (ROS), as well as neutralized the damaging effects of H2O2 in mitochondria energy-producing and cell metabolism. Pre-treatment of H2S also decreased H2O2-induced suppression of endogenous H2S production enzymes, cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE), and 3-mercapto-pyruvate sulfurtransferase (MPST). Furthermore, the administration of H2S attenuated [Ca2+] overload and endoplasmic reticulum (ER) stress through the mitogen-activated protein kinase (MAPK) signaling pathway. Therefore, H2S might be a potential therapeutic agent for reducing ROS and ER stress-associated apoptosis against H2O2-induced lung injury.

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Carbocisteine attenuates hydrogen peroxide-induced inflammatory injury in A549 cells via NF-κB and ERK1/2 MAPK pathways

International Immunopharmacology ◽

10.1016/j.intimp.2014.12.018 ◽

2015 ◽

Vol 24 (2) ◽

pp. 306-313 ◽

Cited By ~ 15

Author(s):

Wei Wang ◽

Jin-ping Zheng ◽

Shao-xuan Zhu ◽

Wei-jie Guan ◽

Mao Chen ◽

...

Keyword(s):

Hydrogen Peroxide ◽

A549 Cells ◽

Inflammatory Injury ◽

Mapk Pathways

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Fe-Hemin-Metal Organic Frameworks/Three-Dimensional Graphene Composites with Efficient Peroxidase-Like Bioactivity for Real-Time Electrochemical Detection of Extracellular Hydrogen Peroxide

Journal of The Electrochemical Society ◽

10.1149/1945-7111/ac3b04 ◽

2021 ◽

Author(s):

Shiying Zhou ◽

Human Sun ◽

Xianfeng Wang ◽

Peng Lu ◽

Danqun Huo ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Real Time ◽

Metal Organic Frameworks ◽

Three Dimensional ◽

A549 Cells ◽

Dynamic Monitoring ◽

Serum Samples ◽

Time Dynamic ◽

Metal Organic ◽

Time Determination

Abstract Real-time detection of extracellular hydrogen peroxide is important for dynamic monitoring of diseases and cytopathological research. Here, a novel composite of Fe-hemin-metal organic frameworks/three-dimensional graphene (Fe-hemin MOFs/3DG) was prepared by embedding hemin into amino-contained Fe-MOFs, then decorated with 3DG. The obtained Fe-hemin MOFs/3DG possessed efficient peroxidase-like bioactivity and could serve as an effective catalyst for construction of H2O2 electrochemical sensor. The electrochemical results show that the proposed sensor based on Fe-hemin MOFs/3DG has excellent catalytic activity for H2O2. With a linear range was 10 - 12080 μM and LOD was 0.34 μM, this sensor showed favorable selectivity, repeatability and stability, which could be used to detect H2O2 in real serum samples. Most importantly, this sensor realized the real-time determination of H2O2 released by A549 cells and possessed good biocompatibility. The outstanding electrochemical performance mainly benefited from the unique porous structure of MOFs, which could effectively protect the active center of hemin, and the introduction of 3DG greatly improved the conductivity of Fe-hemin MOFs. Therefore, the Fe-hemin MOFs/3DG could be a promising probe for real-time dynamic monitoring of H2O2.

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Argon Preconditioning Protects Airway Epithelial Cells against Hydrogen Peroxide-Induced Oxidative Stress

European Surgical Research ◽

10.1159/000448682 ◽

2016 ◽

Vol 57 (3-4) ◽

pp. 252-262 ◽

Cited By ~ 4

Author(s):

Christina Hafner ◽

Hong Qi ◽

Lourdes Soto-Gonzalez ◽

Katharina Doerr ◽

Roman Ullrich ◽

...

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Protein Kinase ◽

Epithelial Cells ◽

Apoptotic Cell ◽

A549 Cells ◽

Airway Epithelial Cells ◽

Cerebral Injury ◽

Mitogen Activated Protein Kinase ◽

Airway Epithelial

Background: Oxidative stress is the predominant pathogenic mechanism of ischaemia-reperfusion (IR) injury. The noble gas argon has been shown to alleviate oxidative stress-related myocardial and cerebral injury. The risk of lung IR injury is increased in some major surgeries, reducing clinical outcome. However, no study has examined the lung-protective efficacy of argon preconditioning. The present study investigated the protective effects of argon preconditioning on airway epithelial cells exposed to hydrogen peroxide (H2O2) to induce oxidative stress. Methods: A549 airway epithelial cells were treated with a cytotoxic concentration of H2O2 after exposure to standard air or 30 or 50% argon/21% oxygen/5% carbon dioxide/rest nitrogen for 30, 45 or 180 min. Cells were stained with annexin V/propidium iodide, and apoptosis was evaluated by fluorescence-activated cell sorting. Protective signalling pathways activated by argon exposure were identified by Western blot analysis for phosphorylated candidate molecules of the mitogen-activated protein kinase and protein kinase B (Akt) pathways. Results: Preconditioning with 50% argon for 30, 45 and 180 min and 30% argon for 180 min caused significant protection of A549 cells against H2O2-induced apoptosis, with increases in cellular viability of 5-47% (p < 0.0001). A small adverse effect was also observed, which presented as a 12-15% increase in cellular necrosis in argon-treated groups. Argon exposure resulted in early activation of c-Jun N-terminal kinase (JNK) and p38, peaking 10- 30 min after the start of preconditioning, and delayed activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, peaking after 60-90 min. Conclusions: Argon preconditioning protects airway epithelial cells from H2O2-induced apoptotic cell death. Argon activates the JNK, p38, and ERK1/2 pathways, but not the Akt pathway. The cytoprotective properties of argon suggest possible prophylactic applications in surgery-related IR injury of the lungs.

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Hydrogen Peroxide Causes Cell Death via Increased Transcription of HOXB13 in Human Lung Epithelial A549 Cells

Toxics ◽

10.3390/toxics8040078 ◽

2020 ◽

Vol 8 (4) ◽

pp. 78

Author(s):

Naoki Endo ◽

Takashi Toyama ◽

Akira Naganuma ◽

Yoshiro Saito ◽

Gi-Wook Hwang

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Cell Death ◽

Human Lung ◽

A549 Cells ◽

Protein Levels ◽

Intracellular Ros ◽

Lung Epithelial ◽

Homeobox Protein

Although homeobox protein B13 (HOXB13) is an oncogenic transcription factor, its role in stress response has rarely been examined. We previously reported that knockdown of HOXB13 reduces the cytotoxicity caused by various oxidative stress inducers. Here, we studied the role of HOXB13 in cytotoxicity caused by hydrogen peroxide in human lung epithelial A549 cells. The knockdown of HOXB13 reduced hydrogen peroxide-induced cytotoxicity; however, this phenomenon was largely absent in the presence of antioxidants (Trolox or N-acetyl cysteine (NAC)). This suggests that HOXB13 may be involved in the cytotoxicity caused by hydrogen peroxide via the production of reactive oxygen species (ROS). Hydrogen peroxide also increased both the mRNA and protein levels of HOXB13. However, these increases were rarely observed in the presence of a transcriptional inhibitor, which suggests that hydrogen peroxide increases protein levels via increased transcription of HOXB13. Furthermore, cell death occurred in A549 cells that highly expressed HOXB13. However, this cell death was mostly inhibited by treatment with antioxidants. Taken together, our findings indicate that HOXB13 may be a novel factor involved in the induction of oxidative stress, which causes cell death via intracellular ROS production.

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