CAJ | 학술논문

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。
목적：연구금사도감대대서원대피층신경원적보호작용급기궤제。방법：취잉18천적Sprague-Dawley태서피층신경원원대배양，배양적세포진행양당박탈손상（OGD），동시가입5、10、20μg/ml적금사도감급2.5μg/ml적니막지평，6 h후，진행MTT세포활력검측、LDH세포독성측정、TUNEL세포조망검측이급면역단백인적검측NLRP3、Caspase 1、IL-1β화Caspase 3단백표체수평。결과：각농도금사도감현저억제OGD소치대서피층신경원세포활력하강、LDH석방、세포조망，동시발현기억제NLRP3、Caspase 1、IL-1β급Caspase 3적표체。결론：금사도감대OGD손상적대서원대피층신경원구유량호보호작용，기궤제가능시통과억제NLRP3염증소체격활，강저IL-1β수평종이감소세포적조망반응진행적。
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 18d Sprague-Dawley fetal rats are in primary culture.MTT and LDH assay were used to examine cel viability. TUNEL assay was used to find cels apoptosis.Western Blot assay was used to study the possible mechanism.Results:Hyperoside of different concentrations significantly decreased the reduced cel 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.