Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 614, Issue 1-3, Pages 58-65Publisher
ELSEVIER
DOI: 10.1016/j.ejphar.2009.04.056
Keywords
Oxidative injury; Lindera strychnifolia; HT22; Neuroprotective; Heme oxygenase-1; Nrf2 (nuclear factor-E2-related factor 2) nuclear translocation; Antioxidant response element; ERK (extracellular signal-regulated kinase) phosphorylation
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Funding
- Ministry of Health & Welfare, Republic of Korea [B03-0009-AM0804-07A5-00030B]
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Oxidative injury contributes to neuronal degeneration in many central nervous system (CNS) diseases, such as Parkinson's disease, Alzheimer's disease, epilepsy and ischemia. Inducible heme oxygenase (HO)-1 acts against oxidants that are thought to play a role in the pathogenesis of these diseases. Lindenenyl acetate, isolated by bioassay-guided fractionation of the MeOH extract of the roots of Lindera strychnifolia, showed potent neuroprotective effects on glutamate-induced neurotoxicity by inducing the expression of HO-1 and increasing the activity of HO in mouse hippocampal HT22 cells. Furthermore, lindenenyl acetate caused the nuclear accumulation of nuclear factor-E2-related factor 2 (Nrf2) and increased the promoter activity of antioxidant response elements (ARE) in mouse hippocampal HT22 cells. In addition, we found that treatment of the cells with extracellular signal-regulated kinase (ERK) inhibitor (U0126) reduced lindenenyl acetate-induced HO-1 expression. Lindenenyl acetate also increased ERK phosphorylation. These results suggest that lindenenyl acetate increases cellular resistance to glutamate-induced oxidative injury in mouse hippocampal HT22 cells, presumably through the ERK pathway-Nrf2/ARE-dependent HO-1 expression. (C) 2009 Elsevier B.V. All rights reserved.
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