Neuroprotection against cobalt chloride-induced cell apoptosis of primary cultured cortical neurons by salidroside
Neuroprotection against cobalt chloride-induced cell apoptosis of primary cultured cortical neurons by salidroside
复制标题
红景天苷对氯化钴诱导的原代培养皮质神经元细胞凋亡的神经保护作用
DOI：
10.1007/s11010-011-0815-4
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发表时间：
2011-08-01
影响因子：
4.3
通讯作者：
Ding, Fei
中科院分区：
文献类型：
--
作者：
Zhang, Shuqiang;Chen, Xia;Ding, Fei
红景天苷是一种植物来源的酚糖苷，已被证明具有广泛的药理学特性，包括对不同损伤引起的神经元死亡的保护作用。为了进一步了解红景天苷特有的神经保护功能，本研究使用原代培养的大鼠皮层神经元作为细胞模型，研究红景天苷是否能够预防暴露于缺氧诱导剂氯化钴（CoCl2）后的细胞损伤。 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物试验、Hoechst33342染色、末端脱氧核苷酸转移酶dUTP介导的切口末端标记测定和Bax/Bcl-2比率分析的数据表明，红景天苷预处理以剂量依赖性方式减弱缺氧诱导的原代培养皮质神经元的凋亡细胞死亡。此外，对可能机制的初步探索表明，我们的实验环境中显示的红景天苷的保护作用可能是通过增强缺氧诱导因子-1α的表达、减轻细胞内活性氧水平的增加以及抑制核因子-κB蛋白的过度表达来介导的。
Salidroside, a phenol glycoside of plant origin, has been documented to possess a broad spectrum of pharmacological properties, including protective effects against neuronal death induced by different insults. To provide further insights into the neuroprotective functions peculiar to salidroside, this study used primary cultured cortical neurons of rats as a cell model to examine whether salidroside was able to prevent against cell damage after exposure to cobalt chloride (CoCl2), a hypoxia-inducing agent. The data from 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide test, Hoechst33342 staining, terminal deoxynucleotidyl transferase dUTP-mediated nicked end labeling assay, and Bax/Bcl-2 ratio analysis indicated that salidroside pretreatment attenuated hypoxia-induced apoptotic cell death of primary cultured cortical neurons in a dose-dependent manner. Moreover, preliminary exploration of the possible mechanisms suggested that the protective effects of salidroside, shown in our experimental setting, might probably be mediated by enhancing the expression of hypoxia-inducible factor-1α, alleviating the increase of intracellular reactive oxygen species levels, and inhibiting over-expression of nuclear factor-kappa B protein.