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作 者:魏欢[1,2] 李玲[1] 战丽萍[2] 张波[3] 赵嘉[4] 裴中[1] 黄如训[1]
机构地区:[1]中山大学附属第一医院神经科,广东广州510000 [2]昆明医学院附属延安医院神经科,云南昆明650000 [3]广州医学院附属第二医院神经科,广东广州510000 [4]中山大学附属第二医院神经科,广东广州510000
出 处:《中风与神经疾病杂志》2011年第8期697-700,共4页Journal of Apoplexy and Nervous Diseases
摘 要:目的探讨在糖氧剥夺(OGD)损伤下,丁基苯酞(NBP)对内源性保护因子PGC-1α表达的影响及其可能机制。方法体外培养内皮细胞株,建立糖氧剥夺模型;运用噻唑蓝比色分析法(MTT)检测内皮细胞活性;分光光度法检测内皮细胞一氧化氮合酶(eNOS)活性;免疫荧光(IF)和Western blot(WB)的方法观察PGC-1α表达水平的变化。结果 NBP能使OGD损伤条件下内皮细胞活性上升;而同时加用特异性eNOS抑制剂L-NIO,NBP的这种保护作用消失。较之单纯OGD组,NBP预处理组能使已经增高的eNOS酶活性继续上升。IF及WB的结果均提示,NBP预处理组较单纯OGD组,能进一步增加OGD 6h后PGC-1α的表达,而同时加用特异性eNOS抑制剂后,NBP的这种上调作用减弱。结论 NBP能有效地减轻OGD条件下的血管内皮细胞损伤;上调PGC-1α的表达,达到细胞保护作用,部分是通过保护内皮细胞eNOS酶活性而实现的。Objective To investigate the mechanism that NBP contribute to protect endothelial cells from oxygen-glucose deprivation(OGD) damage.Methods We used SV40-transformed aortic rat endothelial cell line(SVAREC) to establish the OGD model,MTT assay to detect cell viability and the spectrophotometric method to detect eNOS activity.Immunofluorescence and Western Blot methods were used to detect the protein level of PGC-1α.Results After OGD,the cell viability decreased,but NBP could rescue it.But the protective function of NBP was abated by eNOS inhibitor L-NIO.Also NBP could promote the eNOS activity during OGD.From the IF and WB results,we found that the already increased PGC-1α during OGD could be promoted further more by NBP.But the promote function of NBP could be abated by eNOS inhibitor L-NIO.Conclusion It is eNOS through which NBP increase the expression of PGC-1α during OGD.In this way,NBP present its protective function in cell viability and vascular proliferation.
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