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培养的神经胶质细胞中短暂缺氧应激对超氧化物歧化酶(SOD)mRNA和活性的影响。

Modification of superoxide dismutase (SOD) mRNA and activity by a transient hypoxic stress in cultured glial cells.

作者信息

Niu C S, Chang C K, Lin L S, Jou S B, Kuo D H, Liao S S, Cheng J T

机构信息

Department of Pharmacology, Tzu-Chi Junior College of Nursing, Hualien, Taiwan.

出版信息

Neurosci Lett. 1998 Jul 31;251(3):145-8. doi: 10.1016/s0304-3940(98)00506-0.

Abstract

In order to understand the role of superoxide dismutase (SOD) in response to transient hypoxia or hypoxia-reperfusion in astrocytes, the present study performed an in vitro investigation using rat glial cells in culture. Hypoxia was induced by an incubation with nitrogen gas for 10 min and that followed a further reperfusion with air for 10 min was indicating as hypoxia-normoxia. Activity of SOD was determined by the reduction of nitroblue tetrazolium (NTB). Changes of mRNA for Cu,Zn-SOD or Mn-SOD were also characterized using Northern blotting analysis. Transient hypoxia increased the activity of Mn-SOD but not that of Cu,Zn-SOD in glial cells. Expression of mRNA for SOD was also elevated in cells received hypoxia and the mRNA level for Mn-SOD raised higher than that for Cu,Zn-SOD. In cells received hypoxia-reperfusion, these changes of SOD both the activity and the mRNA level were not observed. Otherwise, the SOD protein amount, both Cu,Zn-SOD and Mn-SOD, identified by Western blotting was not changed in glial cells receiving hypoxic stress or not. The obtained results suggest that gene expression and activity of Mn-SOD in glial cells can be activated in response to the transient hypoxic stress.

摘要

为了了解超氧化物歧化酶(SOD)在星形胶质细胞对短暂缺氧或缺氧-复氧反应中的作用,本研究使用培养的大鼠神经胶质细胞进行了一项体外研究。通过用氮气孵育10分钟诱导缺氧,随后再用空气复氧10分钟,这被称为缺氧-常氧。通过硝基蓝四唑(NTB)的还原测定SOD的活性。还使用Northern印迹分析来表征铜锌超氧化物歧化酶(Cu,Zn-SOD)或锰超氧化物歧化酶(Mn-SOD)的mRNA变化。短暂缺氧增加了神经胶质细胞中Mn-SOD的活性,但未增加Cu,Zn-SOD的活性。在经历缺氧的细胞中,SOD的mRNA表达也升高,并且Mn-SOD的mRNA水平升高得比Cu,Zn-SOD更高。在经历缺氧-复氧的细胞中,未观察到SOD在活性和mRNA水平上的这些变化。此外,通过蛋白质印迹法鉴定的Cu,Zn-SOD和Mn-SOD的SOD蛋白量在受到或未受到缺氧应激的神经胶质细胞中均未改变。所获得的结果表明,神经胶质细胞中Mn-SOD的基因表达和活性可响应短暂的缺氧应激而被激活。

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