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KMID : 0545120090190111355
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Journal of Microbiology and Biotechnology
2009 Volume.19 No. 11 p.1355 ~ p.1363
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Astaxanthin Inhibits H2O2-Mediated Apoptotic Cell Death in Mouse Neural Progenitor Cells via Modulation of P38 and MEK Signaling Pathways
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Kim Jeong-Hwan
Choi Woo-Bong
Lee Jong-Hwan
Jeon Seong-Soo
Choi Yung-Hyun
Kim Byung-Woo
Chang Hyo-Ihl
Nam Soo-Wan
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Abstract
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In the present study, neuroprotective effects of astaxanthin on H2O2-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-GSK3beta, 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 H2O2 treatment, caspases activities were prominently increased but astaxanthin pretreatment significantly inhibited H2O2-mediated caspases activation. Astaxanthin pretreatment also significantly recovered ATP production ability of H2O2-treated cells. These findings indicate that astaxanthin inhibits H2O2-mediated apoptotic features in mNPCs. Inhibition assays with SB203580 (10 uM, a specific inhibitor of p38) and PD98059 (10 uM, 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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KEYWORD
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Antioxidant, apoptotic cell death, astaxanthin, H2O2, mouse neural progenitor cells
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