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局灶性脑缺血期间信号转导子和转录激活子(STAT)因子通路的调节:大脑中动脉闭塞后大鼠海马的基因表达阵列研究

Modulation of signal transducers and activators of transcription (STAT) factor pathways during focal cerebral ischaemia: a gene expression array study in rat hippocampus after middle cerebral artery occlusion.

作者信息

Sun Sheng-Li, Li Tie-Jun, Yang Peng-Yuan, Qiu Yan, Rui Yao-Cheng

机构信息

Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai, China.

出版信息

Clin Exp Pharmacol Physiol. 2007 Nov;34(11):1097-101. doi: 10.1111/j.1440-1681.2007.04679.x.

Abstract
  1. Signal transducers and activators of transcription (STAT) factors are a family of transcription factors that mediate intracellular signalling initiated at cytokine cell surface receptors and transmitted to the nucleus. In the present study, we determined the global changes in STAT gene expression in the hippocampus of rats after focal cerebral ischaemia and reperfusion using microarray analysis. 2. The present study used middle cerebral artery occlusion (MCAO) to induce ischaemia and reperfusion in Sprague-Dawley rats. Using superarray Q series Janus tyrosine kinases (Jak)/STAT signalling pathway gene array, a total of 96 genes was screened in adult male rat hippocampus after transient focal cerebral ischaemia. 3. The results showed that 23 genes were upregulated at least twofold by ischaemia treatment and that 12 genes were downregulated at least threefold by ischaemia treatment compared with controls. 4. After confirmation by quantitative real-time polymerase chain reaction, the data suggest that the gene expression of STAT2, 5a, 5b, 6 and suppressor of cytokine signalling (SOCS) 4 was increased by ischaemia, probably due to a compensatory response of the brain, which may play a protective role in damaged brain tissue. 5. The results of the present study provide evidence on global changes in STAT gene expression in the hippocampus of rats after focal cerebral ischaemia and reperfusion, in which STAT2, 5a, 5b, 6 and SOCS4 were confirmed to be significantly modulated during focal cerebral ischaemia.
摘要
  1. 信号转导子和转录激活子(STAT)因子是一类转录因子,它们介导细胞内信号传导,该信号传导起始于细胞因子细胞表面受体,并传递至细胞核。在本研究中,我们使用微阵列分析确定了局灶性脑缺血再灌注后大鼠海马中STAT基因表达的整体变化。2. 本研究采用大脑中动脉闭塞(MCAO)法在Sprague-Dawley大鼠中诱导缺血再灌注。使用超级阵列Q系列Janus酪氨酸激酶(Jak)/STAT信号通路基因阵列,在短暂性局灶性脑缺血后的成年雄性大鼠海马中总共筛选了96个基因。3. 结果显示,与对照组相比,缺血处理使23个基因上调至少两倍,使12个基因下调至少三倍。4. 经定量实时聚合酶链反应确认后,数据表明缺血使STAT2、5a、5b、6和细胞因子信号转导抑制因子(SOCS)4的基因表达增加,这可能是大脑的一种代偿反应,可能对受损脑组织起到保护作用。5. 本研究结果为局灶性脑缺血再灌注后大鼠海马中STAT基因表达的整体变化提供了证据,其中证实STAT2、5a、5b、6和SOCS4在局灶性脑缺血期间受到显著调节。

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