神经损伤与功能重建
神經損傷與功能重建
신경손상여공능중건
NEURAL INJURY AND FUNCTIONAL RECONSTRUCTION
2014年
6期
464-467
,共4页
谢南昌%陈晨%王翠%张倩%夏建华%张宏伟%连亚军
謝南昌%陳晨%王翠%張倩%夏建華%張宏偉%連亞軍
사남창%진신%왕취%장천%하건화%장굉위%련아군
β淀粉样蛋白%小胶质细胞%氧化应激%线粒体分裂蛋白抑制剂
β澱粉樣蛋白%小膠質細胞%氧化應激%線粒體分裂蛋白抑製劑
β정분양단백%소효질세포%양화응격%선립체분렬단백억제제
β-amyloid protein%microglia%oxidative stress%mitochondrial division inhibitor 1
目的：研究线粒体分裂蛋白抑制剂(mdivi-1)能否减轻β淀粉样蛋白（Aβ）诱导的体外原代培养小鼠小胶质细胞的氧化应激损伤。方法：随机将体外原代培养BALB/C小鼠小胶质细胞分为con组、Aβ组、mdi组和 Aβ+mdi 组，con 组不予处理，Aβ组中加入 Aβ，mdi 组中加入 mdivi-1，Aβ+mdi 组分别加入2、5、10、20μmol/L mdivi-1后1 h加入Aβ。分别检测小胶质细胞存活率及凋亡、线粒体膜电位、丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性、8-羟基脱氧鸟苷（8-OHdG）含量。结果：与con组相比，Aβ组小胶质细胞存活率下降，凋亡增加，线粒体膜电位下降，MDA和8-OHdG含量升高，SOD活性下降，差异有统计学意义（＜0.05）；与Aβ组相比，Aβ+mdi组小胶质细胞存活率上升，凋亡减少，线粒体膜电位增加，细胞内MDA和8-OHdG水平下降，SOD活性上升，差异有统计学意义（＜0.05）。结论：mdivi-1对Aβ诱导的体外原代培养小胶质细胞氧化应激损伤具有保护作用。
目的：研究線粒體分裂蛋白抑製劑(mdivi-1)能否減輕β澱粉樣蛋白（Aβ）誘導的體外原代培養小鼠小膠質細胞的氧化應激損傷。方法：隨機將體外原代培養BALB/C小鼠小膠質細胞分為con組、Aβ組、mdi組和 Aβ+mdi 組，con 組不予處理，Aβ組中加入 Aβ，mdi 組中加入 mdivi-1，Aβ+mdi 組分彆加入2、5、10、20μmol/L mdivi-1後1 h加入Aβ。分彆檢測小膠質細胞存活率及凋亡、線粒體膜電位、丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性、8-羥基脫氧鳥苷（8-OHdG）含量。結果：與con組相比，Aβ組小膠質細胞存活率下降，凋亡增加，線粒體膜電位下降，MDA和8-OHdG含量升高，SOD活性下降，差異有統計學意義（＜0.05）；與Aβ組相比，Aβ+mdi組小膠質細胞存活率上升，凋亡減少，線粒體膜電位增加，細胞內MDA和8-OHdG水平下降，SOD活性上升，差異有統計學意義（＜0.05）。結論：mdivi-1對Aβ誘導的體外原代培養小膠質細胞氧化應激損傷具有保護作用。
목적：연구선립체분렬단백억제제(mdivi-1)능부감경β정분양단백（Aβ）유도적체외원대배양소서소효질세포적양화응격손상。방법：수궤장체외원대배양BALB/C소서소효질세포분위con조、Aβ조、mdi조화 Aβ+mdi 조，con 조불여처리，Aβ조중가입 Aβ，mdi 조중가입 mdivi-1，Aβ+mdi 조분별가입2、5、10、20μmol/L mdivi-1후1 h가입Aβ。분별검측소효질세포존활솔급조망、선립체막전위、병이철（MDA）함량、초양화물기화매（SOD）활성、8-간기탈양조감（8-OHdG）함량。결과：여con조상비，Aβ조소효질세포존활솔하강，조망증가，선립체막전위하강，MDA화8-OHdG함량승고，SOD활성하강，차이유통계학의의（＜0.05）；여Aβ조상비，Aβ+mdi조소효질세포존활솔상승，조망감소，선립체막전위증가，세포내MDA화8-OHdG수평하강，SOD활성상승，차이유통계학의의（＜0.05）。결론：mdivi-1대Aβ유도적체외원대배양소효질세포양화응격손상구유보호작용。
Objective:To investigate whether mitochondrial division inhibitor 1 (mdivi-1) attenuates β-amyloid protein (Aβ)-induced oxidative stress injury in primary microglial cells. Methods:Primary microglial cells were randomly divided into control group, Aβgroup, mdivi-1 group and Aβ+mdivi-1 group. The viability and apoptosis of cells, mitochondrial membrane potential, malondialdehyde (MDA) content, superoxide dismutase (SOD) content and 8-hydroxy-deoxyguanosine (8-OHdG) were examined. Results:Compared with control group, the cell viability of Aβ group was significantly reduced, the apoptotic cells was increased, the mitochondrial membrane potential and SOD activity were decreased, while the levels of MDA and 8-OHdG were increased( <0.05). Compared with the Aβgroup, in the Aβ+mdivi-1 group, the cell viability was increased, the apoptotic cells was decreased, the mitochondrial membrane potential and SOD activity were increased, while the levels of MDA and 8-OhdG were decreased ( <0.05). Conclusion:Mdivi-1 exerts neuroprotective effects against Aβ-induced oxida-tive stress injury in primary microglial cells.
