Neolignans from Aristolochia fordiana Prevent Oxidative Stress-Induced Neuronal Death through Maintaining the Nrf2/HO-1 Pathway in HT22 Cells

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• 作者：Gui-Hua Tang ; Zi-Wei Chen ; Ting-Ting Lin ; Min Tan ; Xiao-Yun Gao ; Jing-Mei Bao ; Zhong-Bin Cheng ; Zhang-Hua Sun ; Gang Huang ; Sheng Yin
• 刊名：Journal of Natural Products
• 出版年：2015
• 出版时间：August 28, 2015
• 年：2015
• 卷：78
• 期：8
• 页码：1894-1903
• 全文大小：652K
• ISSN：1520-6025

文摘

Bioassay-guided fractionation of the ethanolic extract of the stems of Aristolochia fordiana led to the isolation of six new dihydrobenzofuran neolignans (1鈥?b>3 and 7鈥?b>9), three new 2-aryldihydrobenzofurans (4鈥?b>6), a new 8-O-4鈥?neolignan (10), and 14 known analogues (11鈥?b>24). The structures of compounds 1鈥?b>10 were established by spectroscopic methods, and their absolute configurations were determined by analyses of the specific rotation and electronic circular dichroism data. The neuroprotective effects of compounds 1鈥?b>24 against glutamate-induced cell death were tested in hippocampal neuronal cell line HT22. Compounds 17 and 20鈥?b>24 exhibited moderate neuroprotective activity by increasing the endogenous antioxidant defense system. In addition, the neolignans activated the Nrf2 (nuclear factor E2-related factor 2) pathway, resulting in the increase of the expression of endogenous antioxidant protein HO-1 (heme oxygenase-1). The active compounds also preserved the levels of antiapoptotic protein Bcl-2 (B cell lymphoma/leukemia-2), which was decreased by glutamate. Collectively, these results suggested that the active neolignans protect neurons against glutamate-induced cell death through maintaining the Nrf2/HO-1 signaling pathway as well as preserving the Bcl-2 protein and might be promising novel beneficial agents for oxidative stress-associated diseases.