Astaxanthin Inhibits H₂O₂-Mediated Apoptotic Cell Death in Mouse Neural Progenitor Cells via Modulation of P38 and MEK Signaling Pathways
2009
Kim, J.H., Dong-Eui University, Busan, Republic of Korea | Choi, W.B., Dong-Eui University, Busan, Republic of Korea | Lee, J.H., Dong-Eui University, Busan, Republic of Korea | Jeon, S.J., Dong-Eui University, Busan, Republic of Korea | Choi, Y.H., Dong-Eui University, Busan, Republic of Korea | Kim, B.W., Dong-Eui University, Busan, Republic of Korea | Chang, H.I., Korea University, Seoul, Republic of Korea | Nam, S.W., Dong-Eui University, Busan, Republic of Korea
In the present study, the 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-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 H₂O₂ treatment, caspases activities were prominently increased, but astaxanthin pretreatment significantly inhibited H₂O₂-mediated caspases activation. Astaxanthin pretreatment also significantly recovered the ATP production ability of H₂O₂-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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