CAJ | 학술논문

目的从蛋白质水平研究丁苯酞对连二亚硫酸钠(Na2S2O4)致PC12细胞缺氧的保护作用及其作用机制. 方法利用含Na2S2O4的无血清培养基处理PC12细胞,建立细胞缺氧模型,并观察丁苯酞对细胞缺氧的保护作用.噻唑盐比色法(MTT)测定细胞活性,蛋白质组学技术鉴定差异表达蛋白. 结果随着丁苯酞浓度的增大,细胞平均吸光度(A)值逐渐增加.当丁苯酞浓度大于等于5 mol/L时,细胞平均A值与未添加丁苯酞的模型组细胞A值差异有统计学意义(P＜0.05).蛋白质组学技术鉴定出PC12细胞缺氧模型组与丁苯酞干预组共17个差异表达蛋白点,多为细胞骨架蛋白、凋亡相关蛋白及氧化应激相关蛋白等. 结论丁苯酞可减少缺氧导致的神经元凋亡.细胞骨架蛋白、凋亡相关蛋白及氧化应激相关蛋白可能在丁苯酞的神经保护机制中发挥作用.
목적 종단백질수평연구정분태대련이아류산납(Na2S2O4)치PC12세포결양적보호작용급기작용궤제. 방법 이용함Na2S2O4적무혈청배양기처리PC12세포,건립세포결양모형,병관찰정분태대세포결양적보호작용.새서염비색법(MTT)측정세포활성,단백질조학기술감정차이표체단백. 결과수착정분태농도적증대,세포평균흡광도(A)치축점증가.당정분태농도대우등우5 mol/L시,세포평균A치여미첨가정분태적모형조세포A치차이유통계학의의(P＜0.05).단백질조학기술감정출PC12세포결양모형조여정분태간예조공17개차이표체단백점,다위세포골가단백、조망상관단백급양화응격상관단백등. 결론 정분태가감소결양도치적신경원조망.세포골가단백、조망상관단백급양화응격상관단백가능재정분태적신경보호궤제중발휘작용.
Objective To explore the protective effect and molecular mechanism of dl-3-n-butylphthalide (NBP) against oxygen-glucose deprivation induced by sodium hydrosulfite in PC12 cells at proteomic level.Methods PC12 cells impaired by serum-free culture media with sodium hydrosulfite were used as the cell models ofhypoxia,and the protective effects of NBP on hypoxic cells were observed.Methyl thiazolyl tetrazolium (MTT) assay was used to measure the viabilities of PC12 cells.Proteomic technique was employed to identify the differential expression proteins.Results Following the increment of NBP concentrations,the cell absorbance (A) value increased gradually (the PC12 cell apoptosis reduced gradually); when the NBP concentration reached 5 mol/L,their cell A value was significantly different as compared with that of cells without adding NBP (P＜0.05).By using proteomics methods,17 differentially-expressed protein spots in the cells without adding NBP and cells with NBP were identified; most of proteins were cytoskeleton proteins,apoptosis related proteins and oxidative stress related proteins.Conclusion NBP can reduce neuronal apoptosis induced by hypoxia,and cytoskeletal proteins,apoptosis-related proteins and oxidative stress related proteins may role in protection of NBP on ischemic neurons.