scholarly journals Mitochondrial Peptide Humanin Protects Silver Nanoparticles-Induced Neurotoxicity in Human Neuroblastoma Cancer Cells (SH-SY5Y)

2019 ◽  
Vol 20 (18) ◽  
pp. 4439 ◽  
Author(s):  
Gurunathan ◽  
Jeyaraj ◽  
Kang ◽  
Kim
Keyword(s):  
Oxidative Stress ◽  
Silver Nanoparticles ◽  
Protective Effect ◽  
Anticancer Agents ◽  
Membrane Integrity ◽  
Neuroblastoma Cells ◽  
Human Beings ◽  
Human Neuroblastoma ◽  
Cellular Effects ◽  
Harmful Effects

The extensive usage of silver nanoparticles (AgNPs) as medical products such as antimicrobial and anticancer agents has raised concerns about their harmful effects on human beings. AgNPs can potentially induce oxidative stress and apoptosis in cells. However, humanin (HN) is a small secreted peptide that has cytoprotective and neuroprotective cellular effects. The aim of this study was to assess the harmful effects of AgNPs on human neuroblastoma SH-SY5Y cells and also to investigate the protective effect of HN from AgNPs-induced cell death, mitochondrial dysfunctions, DNA damage, and apoptosis. AgNPs were prepared with an average size of 18 nm diameter to study their interaction with SH-SY5Y cells. AgNPs caused a dose-dependent decrease of cell viability and proliferation, induced loss of plasma-membrane integrity, oxidative stress, loss of mitochondrial membrane potential (MMP), and loss of ATP content, amongst other effects. Pretreatment or co-treatment of HN with AgNPs protected cells from several of these AgNPs induced adverse effects. Thus, this study demonstrated for the first time that HN protected neuroblastoma cells against AgNPs-induced neurotoxicity. The mechanisms of the HN-mediated protective effect on neuroblastoma cells may provide further insights for the development of novel therapeutic agents against neurodegenerative diseases.

Impact of glutamine on the effect of neopterin in methyl mercury-exposed neurons

Pteridines ◽  
2016 ◽  
Vol 29 (1) ◽  
pp. 104-113
Author(s):  
Ayse Basak Engin ◽  
Evren Doruk Engin
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Cell Viability ◽  
Methyl Mercury ◽  
Neuroblastoma Cells ◽  
Neuronal Cell ◽  
Cytotoxic Agents ◽  
Glutamine Supplementation ◽  
Human Neuroblastoma ◽  
Ifn Gamma

AbstractExposure to methyl mercury (MeHg), induces blood-brain barrier damage leading to non-selective influx of cytotoxic agents, besides the entrance of inflammatory cells into the brain. However, there is no data available regarding the effects of co-treatment of neopterin and interferon-gamma (IFN-gamma) in MeHgexposed SH-SY5Y dopaminergic neurons. MeHg-exposed SH-SY5Y human neuroblastoma cells were treated with neopterin and IFN-gamma in the presence and absence of L-Glutamine. Cell viability was determined by MTT assay. Oxidative stress intensity coefficient was calculated by taking into consideration the amount of nitric oxide production per viable neuron. 5μM MeHg was found to be more toxic than 1μM or 2μM doses of MeHg for SH-SY5Y cells in glutamine-containing medium. Furthermore, 0.1μM neopterin supplementation significantly increased the neuronal cell viability while, oxidative stress significantly decreased. Glutamine supplementation in culture medium, not only enhanced the MeHg toxicity, but also supported the antioxidant effect of neopterin. These results indicate that neopterin has a protective effect on MeHg toxicity in SH-SY5Y neurons. Neopterin was more effective in improving the total mitochondrial metabolic activity of cells exposed to 5μM MeHg in comparison to IFN-gamma. Although IFN-gamma supplementation alone partially improved 5μM MeHg toxicity on neurons, it weakened the protective effect of neopterin.

scholarly journals 4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Amnah M. Alshangiti ◽  
Eszter Tuboly ◽  
Shane V. Hegarty ◽  
Cathal M. McCarthy ◽  
Aideen M. Sullivan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cytotoxic Effect ◽  
Neuroblastoma Cells ◽  
Reactive Oxygen ◽  
Prognostic Indicator ◽  
Oxygen Species ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.

scholarly journals Protective effect of 1950 MHz electromagnetic field in human neuroblastoma cells challenged with menadione

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Stefano Falone ◽  
Anna Sannino ◽  
Stefania Romeo ◽  
Olga Zeni ◽  
Silvano Santini ◽  
...  
Keyword(s):  
Electromagnetic Field ◽  
Protective Effect ◽  
Neuroblastoma Cells ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

scholarly journals Emodin Alleviates Hydrogen Peroxide-Induced Inflammation and Oxidative Stress via Mitochondrial Dysfunction by Inhibiting the PI3K/mTOR/GSK3β Pathway in Neuroblastoma SH-SY5Y Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Rui Li ◽  
Wenzhou Liu ◽  
Li Ou ◽  
Feng Gao ◽  
Min Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Cell Damage ◽  
Neuroblastoma Cells ◽  
Inflammatory Factors ◽  
Protective Mechanism ◽  
Human Neuroblastoma ◽  
Induced Apoptosis

Emodin is an active monomer extracted from rhubarb root, which has many biological functions, including anti-inflammation, antioxidation, anticancer, and neuroprotection. However, the protective effect of emodin on nerve injury needs to be further elucidated. The purpose of this study is to investigate the effect of emodin on the neuroprotection and the special molecular mechanism. Here, the protective activity of emodin inhibiting H2O2-induced apoptosis and neuroinflammation as well as its molecular mechanisms was examined using human neuroblastoma cells (SH-SY5Y cells). The results showed that emodin significantly enhanced cell viability, reduced cell apoptosis and LDH release. Simultaneously, emodin downregulated H2O2-induced inflammatory factors, including IL-6, NO, and TNF-α, and alleviated H2O2-induced oxidative stress and mitochondrial dysfunction in SH-SY5Y cells. In addition, emodin inhibited the activation of the PI3K/mTOR/GSK3β signaling pathway. What is more, the PI3K/mTOR/GSK3β pathway participated in the protective mechanism of emodin on H2O2-induced cell damage. Collectively, it suggests that emodin alleviates H2O2-induced apoptosis and neuroinflammation potentially by regulating the PI3K/mTOR/GSK3β signaling pathway.

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