欢迎来到《四川大学学报(医学版)》
王盛兰, 但齐琴, 荣荣等. 脑缺血大鼠肺组织中MEK的表达变化[J]. 四川大学学报(医学版), 2012, 43(6): 904-907.
引用本文: 王盛兰, 但齐琴, 荣荣等. 脑缺血大鼠肺组织中MEK的表达变化[J]. 四川大学学报(医学版), 2012, 43(6): 904-907.
WANG Sheng-lan, DAN Qi-qin, RONG Rong. et al. Expression Changes of MEK in Lung of Rats Subjected to Brain Ischemia[J]. Journal of Sichuan University (Medical Sciences), 2012, 43(6): 904-907.
Citation: WANG Sheng-lan, DAN Qi-qin, RONG Rong. et al. Expression Changes of MEK in Lung of Rats Subjected to Brain Ischemia[J]. Journal of Sichuan University (Medical Sciences), 2012, 43(6): 904-907.

脑缺血大鼠肺组织中MEK的表达变化

Expression Changes of MEK in Lung of Rats Subjected to Brain Ischemia

  • 摘要: 目的 探讨脑缺血大鼠肺组织中丝裂原细胞外激酶(MEK)基因、蛋白的表达变化,为了解MEK在脑缺血肺损伤中的作用提供实验依据。方法 成年SD大鼠,随机分为假手术组和脑缺血肺损伤组。用线栓塞大鼠大脑中动脉建立脑缺血模型,假手术组仅分离大脑中动脉不进行栓塞。分别于手术后3 d处死。每组5只大鼠取肺组织进行HE染色、8只大鼠肺组织分别采用RT-PCR及Western blot检测MEK的表达变化。结果 脑缺血后肺组织炎性细胞浸润,MEK mRNA在脑缺血肺损伤组表达明显高于假手术组(P<0.05)。MEK蛋白水平亦较假手术组升高,两组相比,差异有统计学意义(P<0.05)。结论 脑缺血大鼠肺损伤后肺组织MEK表达明显上调,提示MEK信号可能在脑缺血肺损伤中发挥作用。

     

    Abstract: 【Abstract】 Objective To explore the expression changes of mitogen extracellular kinase (MEK) in injured lung after brain ischemia in rats. Methods Adult SD rats were assigned randomly to sham operation group and brain ischemia lung injury (BILI) group. Rats in BILI group were subjected brain ischemia and allowed to survived 3 d. Pathalogical changes in lung were indicated by HE staining. The MEK expression was determined by RT-PCR and Western blot technique. Results After brain ischemia, the bulk of inflammatory cells invaded into lung were observed. Upregulated level of MEK mRNA and protein were found at 3 days after ischemia (P<0.05). Conclusion The upregulated expression of MEK implied that the MEK may play some roles in lung injury after brain ischemia.

     

© 2012 《四川大学学报(医学版)》编辑部 版权所有 cc

开放获取 本文遵循知识共享署名—非商业性使用4.0国际许可协议(CC BY-NC 4.0),允许第三方对本刊发表的论文自由共享(即在任何媒介以任何形式复制、发行原文)、演绎(即修改、转换或以原文为基础进行创作),必须给出适当的署名,提供指向本文许可协议的链接,同时标明是否对原文作了修改;不得将本文用于商业目的。CC BY-NC 4.0许可协议详情请访问 https://creativecommons.org/licenses/by-nc/4.0

/

返回文章
返回