首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >3,4-Dihydroxybenzoic acid from Smilacis chinae rhizome protects amyloid beta protein (25-35)-induced neurotoxicity in cultured rat cortical neurons.
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3,4-Dihydroxybenzoic acid from Smilacis chinae rhizome protects amyloid beta protein (25-35)-induced neurotoxicity in cultured rat cortical neurons.

机译:Smilacis chinae根茎的3,4-二羟基苯甲酸可保护淀粉样β蛋白(25-35)对培养的大鼠皮质神经元的神经毒性。

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摘要

The neuroprotective effect of 3,4-dihydroxybenzoic acid (3,4-DHBA) isolated from Smilacis chinae rhizome against Abeta (25-35)-induced neurotoxicity on cultured rat cortical neurons was found in this study. The protective effect of 3,4-DHBA against Abeta (25-35)-induced neuronal cell death was investigated by measuring cell viability via a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. 3,4-DHBA (1 and 10muM) concentration-dependently inhibited 10muM Abeta (25-35)-induced neuronal apoptotic death. 3,4-DHBA (1 and 10muM) inhibited 10muM Abeta (25-35)-induced elevation of cytosolic Ca(2+) concentration ([Ca(2+)](c)), which was measured by a fluorescent dye, Fluo-4 AM. 3,4-DHBA also inhibited glutamate release into medium, reactive oxygen species (ROS) generation, and caspase-3 activation, which were induced by 10muM Abeta (25-35). These results suggest that 3,4-DHBA prevents Abeta (25-35)-induced neuronal cell damage by interfering with the increase of [Ca(2+)](c), and then by inhibiting glutamate release, generation of ROS and caspase-3 activity.
机译:这项研究发现从from草根茎分离的3,4-二羟基苯甲酸(3,4-DHBA)对Abeta(25-35)诱导的神经毒性对培养的大鼠皮质神经元具有神经保护作用。通过通过3- [4,5-二甲基噻唑-2-基] -2,5-二苯基-四唑鎓测定细胞活力来研究3,4-DHBA对Abeta(25-35)诱导的神经元细胞死亡的保护作用。溴化物(MTT)分析和Hoechst 33342染色。 3,4-DHBA(1和10μM)浓度依赖性抑制10μMAbeta(25-35)诱导的神经元凋亡死亡。 3,4-DHBA(1和10μM)抑制了10μMAbeta(25-35)诱导的胞质Ca(2+)浓度([Ca(2 +)](c))升高,该浓度通过荧光染料测量, Fluo-4 AM。 3,4-DHBA还抑制谷氨酸释放到培养基中,活性氧(ROS)生成和caspase-3激活,这是由10μMAbeta(25-35)诱导的。这些结果表明,3,4-DHBA通过干扰[Ca(2 +)](c)的增加,然后抑制谷氨酸的释放,ROS和caspase的生成来防止Abeta(25-35)诱导的神经元细胞损伤。 -3活动。

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