中国实验诊断学
中國實驗診斷學
중국실험진단학
CHINESE JOURNAL OF LABORATORY DIAGNOSIS
2015年
4期
523-525
,共3页
徐仲航%王一鸣%王勇涛%王姣琦%何金婷%莽靖%邵延坤%徐忠信
徐仲航%王一鳴%王勇濤%王姣琦%何金婷%莽靖%邵延坤%徐忠信
서중항%왕일명%왕용도%왕교기%하금정%망정%소연곤%서충신
ActA/Smads%磷酸化 Smad3%OGD
ActA/Smads%燐痠化 Smad3%OGD
ActA/Smads%린산화 Smad3%OGD
ActA/Smads%phosphorylated Smad3%OGD
目的:探讨磷酸化 Smad3蛋白在神经元样 PC12细胞氧糖剥夺中的表达变化。方法利用鼠神经生长因子(NGF)诱导大鼠嗜铬细胞瘤细胞(PC12)向神经元样细胞转化,应用无糖 DMEM 培养液联合连二亚硫酸钠(Na2 S2 O4)构建氧糖剥夺模型(oxygen-glucose deprivation,OGD),体外模拟神经元缺血性损伤。MTT 检测神经元样细胞 OGD 0,3,6和12 h 存活率,Western blot 检测 OGD 前后磷酸化 Smad3蛋白表达。结果成功建立神经元样PC12细胞的 OGD 模型;OGD 3 h 后细胞存活率显著下降,至 OGD 12 h 降至最低54.7%;细胞内磷酸化 Smad3表达在 OGD 3、6 h 与 OGD 0 h 组相比略升高,至 OGD 12 h 时明显降低。结论磷酸化 Smad3参与在神经元样细胞 OGD早期 ActA/Smads 通路的活化。
目的:探討燐痠化 Smad3蛋白在神經元樣 PC12細胞氧糖剝奪中的錶達變化。方法利用鼠神經生長因子(NGF)誘導大鼠嗜鉻細胞瘤細胞(PC12)嚮神經元樣細胞轉化,應用無糖 DMEM 培養液聯閤連二亞硫痠鈉(Na2 S2 O4)構建氧糖剝奪模型(oxygen-glucose deprivation,OGD),體外模擬神經元缺血性損傷。MTT 檢測神經元樣細胞 OGD 0,3,6和12 h 存活率,Western blot 檢測 OGD 前後燐痠化 Smad3蛋白錶達。結果成功建立神經元樣PC12細胞的 OGD 模型;OGD 3 h 後細胞存活率顯著下降,至 OGD 12 h 降至最低54.7%;細胞內燐痠化 Smad3錶達在 OGD 3、6 h 與 OGD 0 h 組相比略升高,至 OGD 12 h 時明顯降低。結論燐痠化 Smad3參與在神經元樣細胞 OGD早期 ActA/Smads 通路的活化。
목적:탐토린산화 Smad3단백재신경원양 PC12세포양당박탈중적표체변화。방법이용서신경생장인자(NGF)유도대서기락세포류세포(PC12)향신경원양세포전화,응용무당 DMEM 배양액연합련이아류산납(Na2 S2 O4)구건양당박탈모형(oxygen-glucose deprivation,OGD),체외모의신경원결혈성손상。MTT 검측신경원양세포 OGD 0,3,6화12 h 존활솔,Western blot 검측 OGD 전후린산화 Smad3단백표체。결과성공건립신경원양PC12세포적 OGD 모형;OGD 3 h 후세포존활솔현저하강,지 OGD 12 h 강지최저54.7%;세포내린산화 Smad3표체재 OGD 3、6 h 여 OGD 0 h 조상비략승고,지 OGD 12 h 시명현강저。결론린산화 Smad3삼여재신경원양세포 OGD조기 ActA/Smads 통로적활화。
Objective To explore changes of phosphorylated Smad3(p-smad3)expression in neuron-like PC12 cells after oxygen-glucose deprivation(OGD).Methods Rat nerve growth factor (NGF)was used to induce the differentia-tion of rattus PC12 pheochromocytoma cells to neuron-like cells.Na2S2O4 and glucose-free DMEM were introduced to perform an OGD model.The survival rate of cells suffered by OGD was examined by MTT assay.And the protein ex-pression of p-smad3 measured by Western blot.Results PC12 cells were successfully differentiated into neuron-like cells after NGF exposure.The survival rate of cells were dramatically decreased after 3h of OGD exposure,and reached to its lowest point at 12h.Compared with OGD 0h,expression of p-Smad3 was slightly increased after 3 or 6 h,and sig-nificantly decreased at 12h.Conclusion p-Smad3 took part in the activation of ActA/Smads signaling in response to early time of OGD treatment.