Protective effects of sesamin and sesamolin on hypoxic neuronal and PC12 cells

✍ Scribed by Rolis Chien-Wei Hou; Hsueh-Meei Huang; Jason T.C. Tzen; Kee-Ching G. Jeng

• Publisher: John Wiley and Sons
• Year: 2003
• Tongue: English
• Weight: 629 KB
• Volume: 74
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.10749

✦ Synopsis

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 2stress but was diminished in the presence of sesamin and sesamolin. We evaluated further the role of mitogenactivated protein kinases (MAPKs) and caspase-3 in hypoxia-induced PC12 cell death. Extracellular signalregulated 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 apoptoticlike 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.