【作者】 王彩萍； 张小川； 唐妙； 王志伟； 丁斐； 顾晓松；

【Author】 Wang CaiPing;Zhang XiaoChuan;Tang Miao;Ding Fei;Gu XiaoSong;Key Laboratory of Neuroregeneration, Nantong University;

【机构】 南通大学江苏省神经再生重点实验室；

【摘要】 目的:研究金丝桃苷对大鼠原代皮层神经元的保护作用及其机制。方法:取孕18天的Sprague-Dawley胎鼠皮层神经元原代培养,培养的细胞进行氧糖剥夺损伤(OGD),同时加入5、10、20μg/ml的金丝桃苷及2.5μg/ml的尼莫地平,6 h后,进行MTT细胞活力检测、LDH细胞毒性测定、TUNEL细胞凋亡检测以及免疫蛋白印迹检测NLRP3、Caspase 1、IL-1β和Caspase 3蛋白表达水平。结果:各浓度金丝桃苷显著抑制OGD所致大鼠皮层神经元细胞活力下降、LDH释放、细胞凋亡,同时发现其抑制NLRP3、Caspase 1、IL-1β及Caspase 3的表达。结论:金丝桃苷对OGD损伤的大鼠原代皮层神经元具有良好保护作用,其机制可能是通过抑制NLRP3炎症小体激活,降低IL-1β水平从而减小细胞的凋亡反应进行的。更多还原

【Abstract】 Objective: To study the effects and the possible mechanism of hyperoside on primary culture of rat cortical neurons against oxygen-glucose deprivation(OGD) injury. Methods: Cortical neurons of pregnant 18 d Sprague-Dawley fetal rats are in primary culture.MTT and LDH assay were used to examine cell viability. TUNEL assay was used to find cells apoptosis.Western Blot assay was used to study the possible mechanism. Results: Hyperoside of different concentrations significantly decreased the reduced cell viability, LDH release, and TUNEL positive apoptosis induced by OGD injury. Simultaneously, hyperoside could inhibit the upregulated protein level of NLRP3, Caspase 1, IL-1β and Caspase 3 induced by OGD injury. Conclusion: Hyperoside protected primary culture of rat cortical neurons against OGD injury. Furthermore, the neuroprotective effects might be elicited by inhibiting NLRP3, Caspase 1, IL-1β and Caspase 3 to exhibit anti-inflammatory and antiapoptotic effects.更多还原