scholarly journals Iron-Chelated Polydopamine Decorated Doxorubicin-Loaded Nanodevices for Reactive Oxygen Species Enhanced Cancer Combination Therapy

2019 ◽  
Vol 10 ◽  
Author(s):  
Xu-Jing Li ◽  
Wen-Tong Li ◽  
Zi-Hao-Ran Li ◽  
Li-Ping Zhang ◽  
Cheng-Cheng Gai ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Combination Therapy ◽  
Reactive Oxygen ◽  
Oxygen Species

Toxic Reactive Oxygen Species Enhanced Synergistic Combination Therapy by Self-Assembled Metal-Phenolic Network Nanoparticles

2018 ◽  
Vol 30 (8) ◽  
pp. 1704877 ◽  
Author(s):  
Yunlu Dai ◽  
Zhen Yang ◽  
Siyuan Cheng ◽  
Zhongliang Wang ◽  
Ruili Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Combination Therapy ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Synergistic Combination ◽  
Self Assembled

scholarly journals Combination Therapy with Cinnamaldehyde and Hyperthermia Induces Apoptosis of A549 Non-Small Cell Lung Carcinoma Cells via Regulation of Reactive Oxygen Species and Mitogen-Activated Protein Kinase Family

2020 ◽  
Vol 21 (17) ◽  
pp. 6229
Author(s):  
Jinbong Park ◽  
Seung Ho Baek
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Combination Therapy ◽  
Therapeutic Option ◽  
Reactive Oxygen ◽  
Small Cell ◽  
Oxygen Species ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Mitogen Activated Protein

Lung cancer is the largest cause of cancer-induced deaths. Non-small cell lung cancer (NSCLC) is the most frequently observed subtype of lung cancer. Although recent studies have provided many therapeutic options, there is still a need for effective and safe treatments. This paper reports the combined effects of cinnamaldehyde (CNM), a flavonoid from cinnamon, together with hyperthermia, a therapeutic option for cancer treatment, on the A549 NSCLC cell line. A hyperthermia treatment of 43 °C potentiated the cytotoxicity of CNM in A549 cells. This was attributed to an increase in the apoptosis markers and suppression of the survival/protective factors, as confirmed by Western blot assays. Flow cytometry supported this result because the apoptotic profile, cell health profile, and cell cycle profile were regulated by CNM and hyperthermia combination therapy. The changes in reactive oxygen species (ROS) and its downstream target pathway, mitogen-activated protein kinases (MAPK), were evaluated. The CNM and hyperthermia combination increased the generation of ROS and MAPK phosphorylation. N-acetylcysteine (NAC), a ROS inhibitor, abolished the apoptotic events caused by CNM and hyperthermia co-treatment, suggesting that the cytotoxic effect was dependent of ROS signaling. Therefore, we suggest CNM and hyperthermia combination as an effective therapeutic option for the NSCLC treatment.

scholarly journals Tumor-Specific Drug Release and Reactive Oxygen Species Generation for Cancer Chemo/Chemodynamic Combination Therapy

2019 ◽  
Vol 6 (5) ◽  
pp. 1801986 ◽  
Author(s):  
Sheng Wang ◽  
Zhantong Wang ◽  
Guocan Yu ◽  
Zijian Zhou ◽  
Orit Jacobson ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Drug Release ◽  
Combination Therapy ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Specific Drug ◽  
Oxygen Species

scholarly journals In situ formed reactive oxygen species–responsive scaffold with gemcitabine and checkpoint inhibitor for combination therapy

2018 ◽  
Vol 10 (429) ◽  
pp. eaan3682 ◽  
Author(s):  
Chao Wang ◽  
Jinqiang Wang ◽  
Xudong Zhang ◽  
Shuangjiang Yu ◽  
Di Wen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Combination Therapy ◽  
Checkpoint Inhibitor ◽  
Reactive Oxygen ◽  
Oxygen Species

Mitochondria as a source of reactive oxygen species

2009 ◽  
pp. c3 ◽  
Author(s):  
Helena M. Cochemé ◽  
Michael P. Murphy
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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