The Protective Effects of Insulin on Hydrogen Peroxide-Induced Oxidative Stress in C6 Glial Cells

Mahesh, R.; Kim, Sungjin

doi:10.4062/biomolther.2009.17.4.395

Cited by 13 publications

(4 citation statements)

References 50 publications

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“…Therefore, we hypothesized that the protective mechanism of PF on C6 glial cells against H 2 O 2 -induced oxidative damage may be due to its up-regulation of cellular antioxidant system, such as SOD activity, that is capable of scavenging ROS. Li et al [35] reported that PF treatment inhibited production of free radicals by enhancement of SOD activity and reduction of malondialdehyde contents in the brain [36]. In agreement with previous result, our finding showed that treatment of the cells with PF enhanced SOD activity compared to H 2 O 2 -treated control group.…”

Section: Discussionsupporting

confidence: 92%

Protective role of paeoniflorin from hydrogen peroxide-mediated oxidative damage in C6 glial cells

Lee

Nam

Kim

et al. 2020

JABC

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Oxidative stress is one of the pathogenic mechanisms of various neurodegenerative diseases, such as Alzheimer's disease. Neuroglia, the most abundant cells in the brain, is thought to play an important role in the antioxidant defense system and neuronal metabolic support against neurotoxicity and oxidative stress. We investigated the protective effect of paeoniflorin (PF) against oxidative stress in C6 glial cells. Exposure of C6 glial cells to hydrogen peroxide (H 2 O 2 , 500 μM) significantly decreased cell viability and increased amounts of lactate dehydrogenase (LDH) release, indicating H 2 O 2-induced cellular damage. However, treatment with PF significantly attenuated H 2 O 2-induced cell death as shown by increased cell survival and decreased LDH release. The H 2 O 2stimulated reactive oxygen species production was also suppressed, and it may be associated with improvement of superoxide dismutase activity by treatment with PF. In addition, an increase in ratio of Bcl-2/Bax protein expression was observed after treatment with PF. In particular, the downstream of the apoptotic signaling pathway was inhibited in the presence of PF, mostly by reduction of cleaved-poly ADP ribose polymerase, cleaved caspase-3, and-9 protein expression. Furthermore, H 2 O 2-induced phosphorylation of c-Jun N-terminal kinase and extracellular signal-regulated kinase 1/2 was attenuated by treatment with PF. Taken together, neuroprotective effect of PF against oxidative stress probably result from the regulation of apoptotic pathway in C6 glial cells. In conclusion, our findings suggest that PF may be a potent therapeutic agent for neurodegenerative disorders.

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Section: Discussionsupporting

confidence: 92%

Protective role of paeoniflorin from hydrogen peroxide-mediated oxidative damage in C6 glial cells

Lee

Nam

Kim

et al. 2020

JABC

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“…Akt is an initiator of the downstream pathways that inhibit the apoptotic pathways (Chan 2004). Akt also exerts a strong influence on survival of neurons by inhibiting proteins that mediate apoptosis (Kim and Han 2005;Mahesh and Kim 2009). Ras can directly activate PI3-K, an upstream effector for activation of Akt (Chan 2004).…”

Section: Protein Kinase B (Pkb; Akt)mentioning

confidence: 99%

Reactive oxygen/nitrogen species and their functional correlations in neurodegenerative diseases

2012

Self Cite

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The continuous production and efflux of reactive oxygen/nitrogen species from endogenous and exogenous sources can damage biological molecules and initiate a cascade of events. Mitochondria are pivotal in controlling cell survival and death. Cumulative oxidative stress, disrupted mitochondrial respiration, and mitochondrial damage are related with various neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and others. Biochemical cascades of apoptosis are mediated in signaling molecules, including protein kinases and transcription factors. The expressions in the pro-apoptotic signal transduction networks may indeed promote cell death and degeneration in brain cells. The regulation of that protein phosphorylation by kinases and phosphatases is emerging as a prerequisite mechanism in the control of the apoptotic cell death program. In this review, we attempt to put forth the evidence for possible mechanistic explanations for involvement of free radicals in the pathogenesis of neurodegenerative diseases.

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“…After each specific treatment, the cells were treated with MTT solution (1/10 volume of culture medium) and incubated in a 5% CO 2 incubator at 37 • C for 1 h. The absorbance for each reaction product was measured with an ELISA reader (Bio-Rad, Germany) at a wavelength of 450 nm. The results are expressed as the percentage of MTT reduction, with the assumption that the absorbance of the control cells is 100% (Mahesh and Kim, 2009). …”

Section: Determination Of Cell Viabilitymentioning

confidence: 99%

The neuroprotective effect of modified Yeoldahanso-tang via autophagy enhancement in models of Parkinson's disease

Bae

ahn

Chung

et al. 2011

Journal of Ethnopharmacology

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The Protective Effects of Insulin on Hydrogen Peroxide-Induced Oxidative Stress in C6 Glial Cells

Cited by 13 publications

References 50 publications

Protective role of paeoniflorin from hydrogen peroxide-mediated oxidative damage in C6 glial cells

Protective role of paeoniflorin from hydrogen peroxide-mediated oxidative damage in C6 glial cells

Reactive oxygen/nitrogen species and their functional correlations in neurodegenerative diseases

The neuroprotective effect of modified Yeoldahanso-tang via autophagy enhancement in models of Parkinson's disease

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