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Neolignans from Aristolochia fordiana Prevent Oxidative Stress-Induced Neuronal Death through Maintaining the Nrf2/HO-1 Pathway in HT22 Cells
Journal of Natural Products ( IF 3.3 ) Pub Date : 2015-07-30 00:00:00 , DOI: 10.1021/acs.jnatprod.5b00220 Gui-Hua Tang 1 , Zi-Wei Chen 1 , Ting-Ting Lin 1 , Min Tan 2 , Xiao-Yun Gao 3 , Jing-Mei Bao 1 , Zhong-Bin Cheng 1 , Zhang-Hua Sun 1 , Gang Huang 3 , Sheng Yin 1
Journal of Natural Products ( IF 3.3 ) Pub Date : 2015-07-30 00:00:00 , DOI: 10.1021/acs.jnatprod.5b00220 Gui-Hua Tang 1 , Zi-Wei Chen 1 , Ting-Ting Lin 1 , Min Tan 2 , Xiao-Yun Gao 3 , Jing-Mei Bao 1 , Zhong-Bin Cheng 1 , Zhang-Hua Sun 1 , Gang Huang 3 , Sheng Yin 1
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Bioassay-guided fractionation of the ethanolic extract of the stems of Aristolochia fordiana led to the isolation of six new dihydrobenzofuran neolignans (1–3 and 7–9), three new 2-aryldihydrobenzofurans (4–6), a new 8-O-4′ neolignan (10), and 14 known analogues (11–24). The structures of compounds 1–10 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 1–24 against glutamate-induced cell death were tested in hippocampal neuronal cell line HT22. Compounds 17 and 20–24 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.
中文翻译：
来自马兜铃的新木脂素通过维持HT22细胞中的Nrf2 / HO-1途径防止氧化应激诱导的神经元死亡。
生物测定引导的茎的乙醇提取物的分馏马兜铃fordiana导致的六个新的二氢苯并呋喃新木脂体（隔离1 - 3和7 - 9），三个新的2- aryldihydrobenzofurans（4 - 6），一个新的8- ö - 4'新木脂素（10），和14个的已知类似物（11 - 24）。化合物1 – 10的结构通过光谱法确定了它们的绝对构型，并通过分析比旋光度和电子圆二色性数据确定了它们的绝对构型。化合物的神经保护作用1 - 24抗谷氨酸诱导的细胞死亡中海马神经元细胞系HT22进行了测试。化合物17和20 – 24通过增加内源性抗氧化剂防御系统表现出适度的神经保护活性。此外，新木脂素激活了Nrf2（核因子E2相关因子2）途径，导致内源性抗氧化蛋白HO-1（血红素加氧酶-1）的表达增加。活性化合物还保留了抗凋亡蛋白Bcl-2（B细胞淋巴瘤/白血病2）的水平，该水平被谷氨酸降低。总体而言，这些结果表明，活性新木脂素通过维持Nrf2 / HO-1信号通路以及保存Bcl-2蛋白来保护神经元免受谷氨酸诱导的细胞死亡，并且可能是有希望的新型氧化应激相关疾病有益药物。
更新日期：2015-07-30
中文翻译：
来自马兜铃的新木脂素通过维持HT22细胞中的Nrf2 / HO-1途径防止氧化应激诱导的神经元死亡。
生物测定引导的茎的乙醇提取物的分馏马兜铃fordiana导致的六个新的二氢苯并呋喃新木脂体（隔离1 - 3和7 - 9），三个新的2- aryldihydrobenzofurans（4 - 6），一个新的8- ö - 4'新木脂素（10），和14个的已知类似物（11 - 24）。化合物1 – 10的结构通过光谱法确定了它们的绝对构型，并通过分析比旋光度和电子圆二色性数据确定了它们的绝对构型。化合物的神经保护作用1 - 24抗谷氨酸诱导的细胞死亡中海马神经元细胞系HT22进行了测试。化合物17和20 – 24通过增加内源性抗氧化剂防御系统表现出适度的神经保护活性。此外，新木脂素激活了Nrf2（核因子E2相关因子2）途径，导致内源性抗氧化蛋白HO-1（血红素加氧酶-1）的表达增加。活性化合物还保留了抗凋亡蛋白Bcl-2（B细胞淋巴瘤/白血病2）的水平，该水平被谷氨酸降低。总体而言，这些结果表明，活性新木脂素通过维持Nrf2 / HO-1信号通路以及保存Bcl-2蛋白来保护神经元免受谷氨酸诱导的细胞死亡，并且可能是有希望的新型氧化应激相关疾病有益药物。
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