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中国临床药理学与治疗学 ›› 2009, Vol. 14 ›› Issue (10): 1137-1141.

• 基础研究 • 上一篇    下一篇

细胞外信号调节激酶通路对大鼠再灌注损伤肺细胞凋亡的影响

洪加林1, 郑艳蓉2, 石璐3, 贾旭广3, 王万铁3   

  1. 1永嘉县人民医院, 温州 325100, 浙江;
    2温州市疾病预防控制中心, 温州 325027, 浙江;
    3温州医学院病理生理学教研室, 温州 325035, 浙江
  • 收稿日期:2009-08-14 修回日期:2009-10-07 发布日期:2020-10-29
  • 作者简介:洪加林,男,副主任技师。E-mail:zjyjhjl@163.com
  • 基金资助:
    温州市科技局资助项目(Y20070030)

Effect of extracellular signal-regulated kinase on apoptosis of pneumocyte during lung ischemic and reperfusion injury in rats

HONG Jia-lin1, ZHENG Yan-rong2, SHI Lu3, JIA Xu-guang3, WANG Wan-tie3   

  1. 1People' s Hospital of Yongjia, Wenzhou 325100, Zhejiang, China;
    2Center for Disease Prevention and Control of Wenzhou, Wenzhou 325000, Zhejiang, China;
    3Department of Pathophysiology, Wenzhou Medical College, Wenzhou 325035, Zhejiang, China
  • Received:2009-08-14 Revised:2009-10-07 Published:2020-10-29

摘要: 目的 探讨大鼠肺缺血 再灌注损伤时磷酸化细胞外信号调节激酶(ERK) 蛋白表达的变化及其意义。方法 30 只SD 大鼠随机分为三组:假手术对照(C 组), 肺缺血 再灌注(I R 组), 肺缺血再灌注+PD98059(P 组);测定血清丙二醛(MDA)含量、超氧化物岐化酶(SOD) 活力, 免疫组化法检测磷酸化ERK 蛋白的表达;TUNEL 法检测肺组织细胞凋亡的改变;电镜观察肺组织形态学改变。结果 I R 组与C 组比较, MDA 含量明显增加(P<0.01), SOD 活力明显下降(P <0.01), P-ERK 蛋白表达明显上调(P <0.01), 凋亡指数(AI) 显著增高(P <0.01), 肺组织超微结构明显异常;使用ERK 通路特异性抑制剂-PD98059 后,MDA 含量进一步升高(P <0.01), SOD 活力进一步下降(P <0.05), P-ERK 蛋白表达明显下调(P <0.01), AI进一步增加(P <0.01), 肺组织超微结构异常改变继续加重。结论 ERK 信号转导通路可能参与了拮抗再灌注肺细胞凋亡, 对肺缺血 再灌注损伤发挥积极的防治作用。

关键词: 肺, 再灌注损伤, 细胞外信号调节激酶, PD98059, 细胞凋亡

Abstract: AIM: To explore the effect of extracellular signal-regulated kinase (ERK) on apoptosis of pneumocyte during lung ischemic and reperfusion injury in rats. METHODS: 30 rats were randomly divided into three groups:control group(Group C), lung ischemia- reperfusion injury group(Group I R) and PD98059 group(Group P).The content of MDA in serum, the activity of SOD, cell apoptosis index and the p-ERK protein expression were detected by immunohistochemistry, and the ultrastruction changes of lung were observed by electron microscope. RESULTS: Compared with Group C, the content of MDA was increased, the content of SOD was decreased remarkably (all P < 0.01), the expression of p-ERK protein was increased remarkably (P <0.01), and the apoptosis index (AI) was increased in Group I R (P <0.01), abnormal changes of the lung tissue in morphology were observed in Group I R.After PD98059 treatment, the content of MDA was increased (P <0.01), the content of SOD was decreased (P <0.05), the expression of p-ERK protein was decreased(P <0.01), the value of AI was increased(P <0.01), the abnormal changes of the lung tissue in morphology were aggravated markedly. CONCLUSION: The ERK signal transduction pathway maybe protect the lung from the injury caused by ischemia and reperfusion through lessening apoptosis of lung cells in rats.

Key words: lung, reperfusion injury, erk, PD98059, apoptosis

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