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Protective effects of sesamin and sesamolin on hypoxic neuronal and PC12 cells
Author(s) -
Hou Rolis ChienWei,
Huang HsuehMeei,
Tzen Jason T.C.,
Jeng KeeChing G.
Publication year - 2003
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10749
Subject(s) - sesamin , p38 mitogen activated protein kinases , mapk/erk pathway , microbiology and biotechnology , kinase , hypoxia (environmental) , apoptosis , biology , chemistry , pharmacology , biochemistry , oxygen , food science , organic chemistry
Abstract Reactive oxygen species (ROS) are important mediators of a variety of pathological processes, including inflammation and ischemic injury. The neuroprotective effects of sesame antioxidants, sesamin and sesamolin, against hypoxia or H 2 O 2 ‐induced cell injury were evaluated by cell viability or lactate dehydrogenase (LDH) activity. Sesamin and sesamolin reduced LDH release of PC12 cells under hypoxia or H 2 O 2 ‐stress in a dose‐dependent manner. Dichlorofluorescein (DCF)‐sensitive ROS production was induced in PC12 cells by hypoxia or H 2 O 2 ‐stress but was diminished in the presence of sesamin and sesamolin. We evaluated further the role of mitogen‐activated protein kinases (MAPKs) and caspase‐3 in hypoxia‐induced PC12 cell death. Extracellular signal‐regulated protein kinase (ERK) 1, c‐jun N‐terminal kinase (JNK), and p38 MAPKs of signaling pathways were activated during hypoxia. We found that the inhibition of MAPKs and caspase‐3 by sesamin and sesamolin correlated well with the reduction in LDH release under hypoxia. Furthermore, the hypoxia‐induced apoptotic‐like cell death in cultured cortical cells as detected by a fluorescent DNA binding dye was reduced significantly by sesamin and sesamolin. Taken together, these results suggest that the protective effect of sesamin and sesamolin on hypoxic neuronal and PC12 cells might be related to suppression of ROS generation and MAPK activation. © 2003 Wiley‐Liss, Inc.