Astaxanthin inhibits H2O2-mediated apoptotic cell death in mouse neural progenitor cells via modulation of p38 and MEK signaling pathways

Jeong Hwan Kim, Woobong Choi, Jong Hwan Lee, Sung Jong Jeon, Yung Hyun Choi, Byung Woo Kim, Hyo-Ihl Chang, Soo Wan Nam

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

In the present study, the neuroprotective effects of astaxanthin on H 2O2-mediated apoptotic cell death, using cultured mouse neural progenitor cells (mNPCs), were investigated. To cause apoptotic cell death, mNPCs were pretreated with astaxanthin for 8 h and followed by treatment of 0.3 mM H2O2. Pretreatment of mNPCs with astaxanthin significantly inhibited H2O2-mediated apoptosis and induced cell growth in a dose-dependent manner. In Western blot analysis, astaxanthin-pretreated cells showed the activation of p-Akt, p-MEK, p-ERK, and Bcl-2, and the reduction of p-P38, p-SAPK/JNK, Bax, p-GSK3b, cytochrome c, caspase-3, and PARP. Because H2O2 triggers caspases activation, this study examined whether astaxanthin can inhibit caspases activation in H2O2-treated mNPCs. After H 2O2 treatment, caspases activities were prominently increased, but astaxanthin pretreatment significantly inhibited H 2O2-mediated caspases activation. Astaxanthin pretreatment also significantly recovered the ATP production ability of H2O 2-treated cells. These findings indicate that astaxanthin inhibits H2O2-mediated apoptotic features in mNPCs. Inhibition assays with SB203580 (10 μM, a specific inhibitor of p38) and PD98059 (10 μM, a specific inhibitor of MEK) clearly showed that astaxanthin can inhibit H2O2-mediated apoptotic death via modulation of p38 and MEK signaling pathways.

Original languageEnglish
Pages (from-to)1355-1363
Number of pages9
JournalJournal of Microbiology and Biotechnology
Volume19
Issue number11
DOIs
Publication statusPublished - 2009 Nov 1

Fingerprint

Mitogen-Activated Protein Kinase Kinases
Cell Death
Stem Cells
Caspases
astaxanthine
Neuroprotective Agents
p38 Mitogen-Activated Protein Kinases
Caspase 3
Adenosine Triphosphate
Western Blotting
Apoptosis
Growth

Keywords

  • Antioxidant
  • Apoptotic cell death
  • Astaxanthin
  • HO
  • Mouse neural progenitor cells

ASJC Scopus subject areas

  • Biotechnology
  • Applied Microbiology and Biotechnology

Cite this

Astaxanthin inhibits H2O2-mediated apoptotic cell death in mouse neural progenitor cells via modulation of p38 and MEK signaling pathways. / Kim, Jeong Hwan; Choi, Woobong; Lee, Jong Hwan; Jeon, Sung Jong; Choi, Yung Hyun; Kim, Byung Woo; Chang, Hyo-Ihl; Nam, Soo Wan.

In: Journal of Microbiology and Biotechnology, Vol. 19, No. 11, 01.11.2009, p. 1355-1363.

Research output: Contribution to journalArticle

Kim, Jeong Hwan ; Choi, Woobong ; Lee, Jong Hwan ; Jeon, Sung Jong ; Choi, Yung Hyun ; Kim, Byung Woo ; Chang, Hyo-Ihl ; Nam, Soo Wan. / Astaxanthin inhibits H2O2-mediated apoptotic cell death in mouse neural progenitor cells via modulation of p38 and MEK signaling pathways. In: Journal of Microbiology and Biotechnology. 2009 ; Vol. 19, No. 11. pp. 1355-1363.
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abstract = "In the present study, the neuroprotective effects of astaxanthin on H 2O2-mediated apoptotic cell death, using cultured mouse neural progenitor cells (mNPCs), were investigated. To cause apoptotic cell death, mNPCs were pretreated with astaxanthin for 8 h and followed by treatment of 0.3 mM H2O2. Pretreatment of mNPCs with astaxanthin significantly inhibited H2O2-mediated apoptosis and induced cell growth in a dose-dependent manner. In Western blot analysis, astaxanthin-pretreated cells showed the activation of p-Akt, p-MEK, p-ERK, and Bcl-2, and the reduction of p-P38, p-SAPK/JNK, Bax, p-GSK3b, cytochrome c, caspase-3, and PARP. Because H2O2 triggers caspases activation, this study examined whether astaxanthin can inhibit caspases activation in H2O2-treated mNPCs. After H 2O2 treatment, caspases activities were prominently increased, but astaxanthin pretreatment significantly inhibited H 2O2-mediated caspases activation. Astaxanthin pretreatment also significantly recovered the ATP production ability of H2O 2-treated cells. These findings indicate that astaxanthin inhibits H2O2-mediated apoptotic features in mNPCs. Inhibition assays with SB203580 (10 μM, a specific inhibitor of p38) and PD98059 (10 μM, a specific inhibitor of MEK) clearly showed that astaxanthin can inhibit H2O2-mediated apoptotic death via modulation of p38 and MEK signaling pathways.",
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AU - Jeon, Sung Jong

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AU - Kim, Byung Woo

AU - Chang, Hyo-Ihl

AU - Nam, Soo Wan

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AB - In the present study, the neuroprotective effects of astaxanthin on H 2O2-mediated apoptotic cell death, using cultured mouse neural progenitor cells (mNPCs), were investigated. To cause apoptotic cell death, mNPCs were pretreated with astaxanthin for 8 h and followed by treatment of 0.3 mM H2O2. Pretreatment of mNPCs with astaxanthin significantly inhibited H2O2-mediated apoptosis and induced cell growth in a dose-dependent manner. In Western blot analysis, astaxanthin-pretreated cells showed the activation of p-Akt, p-MEK, p-ERK, and Bcl-2, and the reduction of p-P38, p-SAPK/JNK, Bax, p-GSK3b, cytochrome c, caspase-3, and PARP. Because H2O2 triggers caspases activation, this study examined whether astaxanthin can inhibit caspases activation in H2O2-treated mNPCs. After H 2O2 treatment, caspases activities were prominently increased, but astaxanthin pretreatment significantly inhibited H 2O2-mediated caspases activation. Astaxanthin pretreatment also significantly recovered the ATP production ability of H2O 2-treated cells. These findings indicate that astaxanthin inhibits H2O2-mediated apoptotic features in mNPCs. Inhibition assays with SB203580 (10 μM, a specific inhibitor of p38) and PD98059 (10 μM, a specific inhibitor of MEK) clearly showed that astaxanthin can inhibit H2O2-mediated apoptotic death via modulation of p38 and MEK signaling pathways.

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KW - HO

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