CAJ | 학술논문

目的：研究丙戊酸对脑红蛋白表达的影响和机制，及其对双氧水诱导的神经损伤的保护作用。方法 Western blot、RT-PCR和荧光素酶活性实验检测丙戊酸对小鼠和人脑红蛋白表达的影响；荧光素酶活性实验分析CREB在丙戊酸诱导脑红蛋白启动子活性过程中的作用；MTT实验分析丙戊酸对双氧水诱导的神经损伤的保护能力。结果发现丙戊酸上调小鼠和人脑红蛋白的蛋白和mRNA水平，并能上调脑红蛋白基因的启动子活性；CREB特异性抑制剂KG-501和CREB显性负突变体KCREB均抑制丙戊酸诱导脑红蛋白基因的启动子活性；丙戊酸可保护N2 a神经瘤母细胞免受双氧水诱导的损伤。结论 CREB介导了丙戊酸诱导的脑红蛋白表达上调；脑红蛋白可能在丙戊酸保护N2 a细胞免受氧化应激诱导的神经损伤过程中扮演重要作用。
목적：연구병무산대뇌홍단백표체적영향화궤제，급기대쌍양수유도적신경손상적보호작용。방법 Western blot、RT-PCR화형광소매활성실험검측병무산대소서화인뇌홍단백표체적영향；형광소매활성실험분석CREB재병무산유도뇌홍단백계동자활성과정중적작용；MTT실험분석병무산대쌍양수유도적신경손상적보호능력。결과발현병무산상조소서화인뇌홍단백적단백화mRNA수평，병능상조뇌홍단백기인적계동자활성；CREB특이성억제제KG-501화CREB현성부돌변체KCREB균억제병무산유도뇌홍단백기인적계동자활성；병무산가보호N2 a신경류모세포면수쌍양수유도적손상。결론 CREB개도료병무산유도적뇌홍단백표체상조；뇌홍단백가능재병무산보호N2 a세포면수양화응격유도적신경손상과정중분연중요작용。
Aim To investigate the effect and mecha-nism of valproic acid on neuroglobin expression, and the neuroprotective role of valproic acid against H2 O2-induced neurotoxicity. Methods Western blot, RT-PCR and luciferase assay were used to detect the pro-tein levels, mRNA levels and promoter activity of mouse and human neuroglobin induced by valproic acid. Luciferase assay was used to investigate the role of transcription factor CREB in the up-regulation of neuroglobin by valproic acid. MTT assay was used to evaluate the effect of valproic acid against H2 O2-in-duced neurotoxicity. Results VPA treatment marked-ly increased the protein levels, mRNA levels and pro-moter activity of Ngb in mouse N2 a cells and human SKNSH cells. CREB specific inhibitor KG501 or CREB dominant negative mutant KCREB attenuated VPA-induced Ngb promoter activity. VPA could pro-tect N2a cells from H2 O2-induced neurotoxicity. Con-clusion CREB mediates VPA-induced Ngb up-regula-tion, which may contribute to the neuroprotective effects of VPA in oxidative stress in neurons.