[某种物质]乙酸乙酯部位的酚类成分及其对HO诱导的原代皮质神经元细胞凋亡性细胞死亡的神经保护作用。 （注：原文中“from”后面缺少具体物质名称）
Phenolic composition and neuroprotective effects of the ethyl-acetate fraction from against HO-induced apoptotic cell death of primary cortical neuronal cells.
作者信息
Liu Kun, Qi Cuilian, Liu Yihang, Huai Yaping, Hu Huagang, Xiao Xuan, Wang Junpeng
机构信息
College of Biology Science and Engineering, Hebei University of Economics and Business, Shijiazhuang, 050061 Hebei China.
Department of Mathematics and Statistics, Hebei University of Economics and Business, Shijiazhuang, 050061 Hebei China.
出版信息
Food Sci Biotechnol. 2022 Jun 24;31(9):1213-1223. doi: 10.1007/s10068-022-01107-x. eCollection 2022 Aug.
UNLABELLED
The study aimed to characterize phenolic compounds of the 's ethyl-acetate fraction (EAF) and assess the neuroprotective effect of EAF using the HO-treated primary cortical neuronal cells (PCNC) model. Using HPLC-ECD, 5 phenolics were identified and quantified from EAF. HO-treated PCNC experiments in vitro showed that pretreatment with EAF increased the GSH-PX and SOD activities and reduced the NO, MDA, and Aβ contents. Furthermore, EAF suppressed the production of IL-1β, IFN-γ, IL-6, and TNF-α in HO-treated PCNC. Other mechanisms found that EAF reduced Bax, caspase 9, and caspase 3 expressions at the mRNA and protein levels while increasing Bcl-2 expression at the mRNA and protein levels. These results showed that EAF could serve as potential agents for anti-NDD.
SUPPLEMENTARY INFORMATION
The online version contains supplementary material available at 10.1007/s10068-022-01107-x.
未标注
本研究旨在表征[具体物质]的乙酸乙酯馏分（EAF）中的酚类化合物，并使用过氧化氢（HO）处理的原代皮质神经元细胞（PCNC）模型评估EAF的神经保护作用。通过高效液相色谱-电化学检测法（HPLC-ECD），从EAF中鉴定并定量了5种酚类物质。体外HO处理的PCNC实验表明，EAF预处理可提高谷胱甘肽过氧化物酶（GSH-PX）和超氧化物歧化酶（SOD）活性，并降低一氧化氮（NO）、丙二醛（MDA）和β-淀粉样蛋白（Aβ）含量。此外，EAF抑制了HO处理的PCNC中白细胞介素-1β（IL-1β）、干扰素-γ（IFN-γ）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的产生。其他机制发现，EAF在mRNA和蛋白质水平上降低了 Bax、半胱天冬酶9（caspase 9）和半胱天冬酶3（caspase 3）的表达，同时在mRNA和蛋白质水平上增加了Bcl-2的表达。这些结果表明，EAF可作为抗神经退行性疾病（NDD）的潜在药物。
补充信息
在线版本包含可在10.1007/s10068-022-01107-x获取的补充材料。
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