Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells

Chetsawang, Jirapa; Govitrapong, Piyarat; Chetsawang, Banthit

doi:10.1155/2010/803815

Cited by 10 publications

(8 citation statements)

References 16 publications

(17 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our data clearly demonstrate that H 2 O 2 induced a great cell viability lost (by about 40%), in agreement with Chetsawang et al [ 31 ] who found SH-SY5Y cells loss viability mediated by H 2 O 2 . Those authors suggest that Ras protein could be involved in this cell survival decrease.…”

Section: Discussionsupporting

confidence: 93%

Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects

Garcimartín

Merino

González

et al. 2014

BMC Complement Altern Med

View full text Add to dashboard Cite

BackgroundHydrogen peroxide (H2O2) is a toxic agent that induces oxidative stress and cell death. Silicon (Si) is a biological element involved in limiting aluminium (Al) absorption with possible preventive effects in Alzheimer’s disease. However, Si has not yet been associated with other neuroprotective mechanisms.MethodsThe present experiments evaluated in the SH-SY5Y human neuroblastoma cell line the possible role of different Si G5 (50-1000 ng/mL) concentrations in preventing cellular death induced by H2O2 (400 μM, 24 hours).ResultsOur findings showed that H2O2 promoted cell death in the human SH-SY5Y cell cultures and this could be prevented by Si treatment. The loss in cell viability mediated by H2O2 was due to an apoptotic and necrotic process. Apoptotic death was incurred by regulating caspase-8 activity in the extrinsic pathway. The apoptotic and necrotic cell death induced by H2O2 was almost totally reversed by Si (50-500 ng/mL), indicating that it down-regulates both processes in H2O2 treated cells.ConclusionsAccording to our data, Si is able to increase SH-SY5Y cell survival throughout partially blocking cellular damage related to oxidative stress through a mechanism that would affect H2O2/ROS elimination.

show abstract

Section: Discussionsupporting

confidence: 93%

Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects

Garcimartín

Merino

González

et al. 2014

BMC Complement Altern Med

View full text Add to dashboard Cite

show abstract

“…Treatment of ALA in concentration of 1–25 µg/mL to SH-SY5Y cells did not affect cellular conditions in our preliminary study, thus we decided to assess the neuroprotective effect of ALA at a concentration range of 1–25 µg/mL. In agreement with previous studies [ 36 37 ], we observed that SH-SY5Y cells exposed to H 2 O 2 treatment resulted in cell loss. However, treatment with PO and ALA prevented the cell death, as confirmed by the cell viability assay.…”

Section: Discussionsupporting

confidence: 82%

Protective effects of perilla oil and alpha linolenic acid on SH-SY5Y neuronal cell death induced by hydrogen peroxide

et al. 2018

View full text Add to dashboard Cite

BACKGROUND/OBJECTIVEOxidative stress plays a key role in neuronal cell damage, which is associated with neurodegenerative disease. The aim of present study was to investigate the neuroprotective effects of perilla oil (PO) and its active component, alpha-linolenic acid (ALA), against hydrogen peroxide (H2O2)-induced oxidative stress in SH-SY5Y neuronal cells.MATERIALS/METHODSThe SH-SY5Y human neuroblastoma cells exposed to 250 µM H2O2 for 24 h were treated with different concentrations of PO (25, 125, 250 and 500 µg/mL) and its major fatty acid, ALA (1, 2.5, 5 and 25 µ/mL). We examined the effects of PO and ALA on H2O2-induced cell viability, lactate dehydrogenase (LDH) release, and nuclear condensation. Moreover, we determined whether PO and ALA regulated the apoptosis-related protein expressions, such as cleaved-poly ADP ribose polymerase (PARP), cleaved caspase-9 and -3, BCL-2 and BAX.RESULTSTreatment of H2O2 resulted in decreased cell viability, increased LDH release, and increase in the nuclei condensation as indicated by Hoechst 33342 staining. However, PO and ALA treatment significantly attenuated the neuronal cell death, indicating that PO and ALA potently blocked the H2O2-induced neuronal apoptosis. Furthermore, cleaved-PARP, cleaved caspase-9 and -3 activations were significantly decreased in the presence of PO and ALA, and the H2O2-mediated up-regulated BAX/BCL-2 ratio was blocked after treatment with PO and ALA.CONCLUSIONSPO and its main fatty acid, ALA, exerted the protective activity from neuronal oxidative stress induced by H2O2. They regulated apoptotic pathway in neuronal cell death by alleviation of BAX/BCL-2 ratio, and down-regulation of cleaved-PARP and cleaved caspase-9 and -3. Although further studies are required to verify the protective mechanisms of PO and ALA from neuronal damage, PO and ALA are the promising agent against oxidative stress-induced apoptotic neuronal cell death.

show abstract

“…The supernatant was then aspirated off and the formazan crystals were dissolved in 50 μL of DMSO. After 15 min of reaction time, the absorbance was measured at 570 nm using the Omega Star micro plate reader [66]. The experiments were performed in triplicate and the cells viability was expressed as percentages of survival relative to the control sample.…”

Section: Methodsmentioning

confidence: 99%

Olive Biophenols Reduces Alzheimer’s Pathology in SH-SY5Y Cells and APPswe Mice

Omar

Scott

Hamlin

et al. 2018

IJMS

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is a major neurodegenerative disease, associated with the hallmark proteinacious constituent called amyloid beta (Aβ) of senile plaques. Moreover, it is already established that metals (particularly copper, zinc and iron) have a key role in the pathogenesis of AD. In order to reduce the Aβ plaque burden and overcome the side effects from the synthetic inhibitors, the current study was designed to focus on direct inhibition of with or without metal-induced Aβ fibril formation and aggregation by using olive biophenols. Exposure of neuroblastoma (SH-SY5Y) cells with Aβ42 resulted in decrease of cell viability and morphological changes might be due to severe increase in the reactive oxygen species (ROS). The pre-treated SH-SY5Y cells with olive biophenols were able to attenuate cell death caused by Aβ42, copper- Aβ42, and [laevodihydroxyphenylalanine (l-DOPA)] l-DOPA-Aβ42-induced toxicity after 24 h of treatment. Oleuropein, verbascoside and rutin were the major anti-amyloidogenic compounds. Transgenic mice (APPswe/PS1dE9) received 50 mg/kg of oleuropein containing olive leaf extracts (OLE) or control diet from 7 to 23 weeks of age. Treatment mice (OLE) were showed significantly reduced amyloid plaque deposition (p < 0.001) in cortex and hippocampus as compared to control mice. Our findings provide a basis for considering natural and low cost biophenols from olive as a promising candidate drug against AD. Further studies warrant to validate and determine the anti-amyloid mechanism, bioavailability as well as permeability of olive biophenols against blood brain barrier in AD.

show abstract

Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells

Cited by 10 publications

References 16 publications

Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects

Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects

Protective effects of perilla oil and alpha linolenic acid on SH-SY5Y neuronal cell death induced by hydrogen peroxide

Olive Biophenols Reduces Alzheimer’s Pathology in SH-SY5Y Cells and APPswe Mice

Contact Info

Product

Resources

About