Astaxanthin Inhibits H2O2-Mediated Apoptotic Cell Death in Mouse Neural Progenitor Cells via Modulation of P38 and MEK Signaling Pathways

Kim, Jeong Hwan; Choi, Won San; Lee, Jong Hwan; Jeon, Sung Jong; Choi, Yung Hyun; Kim, Byung Woo; Chang, Hyo Ihl; Nam, Soo Woo

doi:10.4014/jmb.0906.06003

Cited by 48 publications

(45 citation statements)

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“…Recently, Lin et al [103] used isolated nerve terminals (synaptosomes) purified from the rat cerebral cortex to investigate the effect of astaxanthin on endogenous glutamate release, and showed that astaxanthin exhibited a dose-dependent inhibition of 4-aminopyridine-elicited release of glutamate, presenting an additional explanation for the neuroprotective effect of astaxanthin besides antioxidant and anti-inflammatory properties. Kim et al [104] found that astaxanthin could inhibit H 2 O 2 -mediated apoptotic death via modulation of p38 and MEK signaling pathways. These results highlighted the therapeutic potential of astaxanthin in the prevention and treatment of a wide range of neurological and neurodegenerative disorders [102,104].…”

Section: Neuroprotective Effectmentioning

confidence: 99%

See 1 more Smart Citation

Potential health‐promoting effects of astaxanthin: A high‐value carotenoid mostly from microalgae

Yuan

Peng

Yin

et al. 2010

Molecular Nutrition Food Res

544

309

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The ketocarotenoid astaxanthin can be found in the microalgae Haematococcus pluvialis, Chlorella zofingiensis, and Chlorococcum sp., and the red yeast Phaffia rhodozyma. The microalga H. pluvialis has the highest capacity to accumulate astaxanthin up to 4-5% of cell dry weight. Astaxanthin has been attributed with extraordinary potential for protecting the organism against a wide range of diseases, and has considerable potential and promising applications in human health. Numerous studies have shown that astaxanthin has potential health-promoting effects in the prevention and treatment of various diseases, such as cancers, chronic inflammatory diseases, metabolic syndrome, diabetes, diabetic nephropathy, cardiovascular diseases, gastrointestinal diseases, liver diseases, neurodegenerative diseases, eye diseases, skin diseases, exercise-induced fatigue, male infertility, and HgCl₂-induced acute renal failure. In this article, the currently available scientific literature regarding the most significant activities of astaxanthin is reviewed.

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Section: Neuroprotective Effectmentioning

confidence: 99%

“…Kim et al [104] found that astaxanthin could inhibit H 2 O 2 -mediated apoptotic death via modulation of p38 and MEK signaling pathways. These results highlighted the therapeutic potential of astaxanthin in the prevention and treatment of a wide range of neurological and neurodegenerative disorders [102,104].…”

Section: Neuroprotective Effectmentioning

confidence: 99%

Potential health‐promoting effects of astaxanthin: A high‐value carotenoid mostly from microalgae

Yuan

Peng

Yin

et al. 2010

Molecular Nutrition Food Res

544

309

View full text Add to dashboard Cite

show abstract

“…*P < 0.05, **P < 0.01, ***P < 0.001 versus control; # P < 0.05, ## P < 0.01, ### P < 0.001 versus VU0155041 group. role in protecting cells from oxidative injury [22,23]. To examine whether JNK and p38 inactivation contributes to the protective effects of mGluR4 on oxidative NSC apoptosis, we further estimated the H 2 O 2 -mediated procaspase-3 cleavage and NSC apoptotic levels in the presence of VU0155041, JNK, or p38 inhibitors.…”

Section: Activation Of Mglur4 Prevented H 2 O 2 -Mediated Cell Death mentioning

confidence: 99%

“…Links between JNK/p38 phosphorylation and cell death upon oxidative stress are well characterized in various types of cells, including neural cells [23,[54][55][56][57]. During experimental oxidative stress-induced cell apoptosis, JNK and p38 were phosphorylated by H 2 O 2 stimulation and caspase cascades in suffered cells were consequently activated, which resulted in cell death [41,[58][59][60], and inhibition of JNK and p38 phosphorylation may play a role in protecting cells against oxidative injuries [22,41,43,54]. We cannot identify if there is crosstalking between the two signal pathways, which may play the synergistic or antistatic roles with each other in oxidative injuries of NSCs.…”

Section: Fig 8 Protective Effect Of Vu0155041 On H 2 O 2 -Inducedmentioning

confidence: 99%

Activation of Type 4 Metabotropic Glutamate Receptor Attenuates Oxidative Stress-Induced Death of Neural Stem Cells with Inhibition of JNK and p38 MAPK Signaling

Zhang

Wang

et al. 2015

Stem Cells and Development

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1Promoting both endogenous and exogenous neural stem cells' (NSCs) survival in the hostile host environments is essential to cell replacement therapy for central nervous system (CNS) disorders. Type 4 metabotropic glutamate receptor (mGluR4), one of the members of mGluRs, has been shown to protect neurons from acute and chronic excitotoxic insults in various brain damages. The present study investigated the preventive effects of mGluR4 on NSC injury induced by oxidative stress. Under challenge with H 2 O 2 , loss of cell viability was observed in cultured rat NSCs, and treatment with selective mGluR4 agonist VU0155041 conferred protective effects against the loss of cellular viability in a concentration-dependent manner, as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Pretreatment of VU0155041 (30 mM) also inhibited the excessive NSC death induced by H 2 O 2 , and group III mGluRs antagonist (RS)-a-methylserine-O-phosphate (MSOP) or gene-targeted knockdown abolished the protective action of mGluR4, indicated by propidium iodide-Hoechst and terminal deoxynucleotidyl transferase-mediated UTP nick end labeling (TUNEL) staining. Western blot assay demonstrated that mGluR4 activation reversed the decreased procaspase-8/9/3and the destructed Bcl-2/Bax expressing balance, and likewise, MSOP and mGluR4 knockdown abrogated the action of mGluR4 activity. Furthermore, inhibition of JNK and p38 mitogen-activated protein kinases (MAPKs) were observed after mGluR4 activation, and as paralleling control, JNK-specific inhibitor SP600125 and p38-specific inhibitor SB203580 significantly rescued the H 2 O 2 -mediated NSC apoptosis and cleavage of procaspase-3. We suggest that activation of mGluR4 prevents oxidative stress-induced NSC death and apoptotic-associated protein activities with involvement of inhibiting the JNK and p38 pathways in cell culture. Our findings may help to develop strategies for enhancing the resided and transplanted NSC survival after oxidative stress insult of CNS.

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“…For example, nanomolar to sub-micromolar concentrations of hydrogen peroxide (H 2 O 2 ) stimulate the proliferation of several cell types, but higher concentrations of H 2 O 2 (>100µM) leads to cell death (Giorgio et al, 2007;Kim et al, 2009;Stone and Yang, 2006). However, the effect of H 2 O 2 is cell type dependent: H 2 O 2 (100µM) increased VSMC proliferation whereas the same concentration inhibits the proliferation of endothelial and fibroblast cells (Rao and Berk, 1992).…”

Section: Intracellular Kinase Pathways Induced By Oxidant Signalling mentioning

confidence: 99%

Non-classical Signalling Mechanisms in Stem Cells

Pébay¹,

Peshavariya²,

Wong³

et al. 2011

Embryonic Stem Cells: The Hormonal Regulation of Pluripotency and Embryogenesis

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Astaxanthin Inhibits H2O2-Mediated Apoptotic Cell Death in Mouse Neural Progenitor Cells via Modulation of P38 and MEK Signaling Pathways

Cited by 48 publications

References 0 publications

Potential health‐promoting effects of astaxanthin: A high‐value carotenoid mostly from microalgae

Potential health‐promoting effects of astaxanthin: A high‐value carotenoid mostly from microalgae

Activation of Type 4 Metabotropic Glutamate Receptor Attenuates Oxidative Stress-Induced Death of Neural Stem Cells with Inhibition of JNK and p38 MAPK Signaling

Non-classical Signalling Mechanisms in Stem Cells

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