Cytoprotective effects of lindenenyl acetate isolated from Lindera strychnifolia

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• 作者：Bin Li ; Gil-Saeng Jeong ; Dae-Gill Kang ; Ho-Sub Lee ; Youn-Chul Kim
• 关键词：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
• 刊名：European Journal of Pharmacology
• 出版年：2009
• 出版时间：1 July 2009
• 年：2009
• 卷：614
• 期：1-3
• 页码：58-65
• 全文大小：796 K

文摘

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.