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中国临床药理学与治疗学 ›› 2005, Vol. 10 ›› Issue (7): 808-811.

• 研究原著 • 上一篇    下一篇

细胞凋亡与肺缺血再灌注损伤的关系及川芎嗪的影响

王晓杨, 王万铁1, 郝茂林1, 张波   

  1. 金华职业技术学院医学院病理生理教研室, 金华321000, 浙江;1温州医学院病理生理教研室, 温州325035, 浙江
  • 收稿日期:2005-04-06 修回日期:2005-06-20 出版日期:2005-07-26 发布日期:2020-11-10
  • 通讯作者: 王万铁, 男, 教授, 硕士生导师, 研究方向:器官缺血再灌注损伤。Tel:(0) 13587688106 E-mail: wzwwt@tom.com
  • 作者简介:王晓杨, 女, 硕士, 副教授。Tel:0579-2472231 E-mail: jhwxy868@sina.com

Relationship between apoptosis and pulmonary ischemia-reperfusion injury in rabbits and intervention of tertram ethylpyrazine

WANG Xiao-yang, WANG Wan-tie1, HAO Mao-ling1, Zhang-Bo   

  1. 1Department of Pathophysiology, the Medical School of Vocational Training College, Jinhua 321000, Zhejiang, China;
    2Department of Pathophysiology, Wenzhou Medical College, Wenzhou 325027, Zhejiang, China
  • Received:2005-04-06 Revised:2005-06-20 Online:2005-07-26 Published:2020-11-10

摘要: 目的: 探讨兔肺组织细胞凋亡和肺缺血再灌注损伤的关系及川芎嗪的影响。方法: 制备兔在体原位肺缺血再灌注损伤模型(PIRI), 应用末端脱氧核苷酸转移酶(TdT) 介导的dUTP 缺口末端标记技术(TUNEL) 检测缺血再灌注损伤所引起的肺细胞凋亡的变化;采用Murata 法进行肺组织损伤定量(IQA) 检测, 进行细胞凋亡与IQA 的相关性分析。结果: 肺缺血再灌注后, 缺血再灌注组(IR 组) 1 、3 和5 h 发生明显的肺细胞凋亡, 凋亡细胞数峰值位于再灌注3 h (P <0.01), 而川芎嗪干预细胞凋亡指数与同一时相缺血再灌注组比较显著降低(P <0.05, P <0.01); IR 组肺组织IQA 值高于TMP 组(P <0.01); 细胞凋亡指数与肺组织损伤定量指标呈正相关(r =0.718, P <0.01) 。结论: 细胞凋亡在肺缺血再灌注损伤机制中可能发挥着重要作用,川芎嗪可减轻肺缺血再灌注导致的细胞凋亡。

关键词: 肺缺血再灌注, 肺组织损伤定量检测, 细胞凋亡, 川芎嗪

Abstract: AIM: To investigate the relationship between apoptosis and pulmonary ischemia-reperfusion injury in rabbits and the intervention of tertram ethylpyrazine. METHODS: An in situ ischemia-reperfusion lung injury rabbit model was established in vivo. Apoptotic cells were explored by the terminal deoxynucleotidyl transferase-mediate dUTP nick-end labelling (TUNEL) technique. The index of quantitative assessment of histologic lung (IQA) was detected by Murata' s way. The correlation was analyzed between the apoptosis and IQA of pulmonary ischemia- reperfusion injury. RESULTS: Obvious apoptosis of pneumocytes occurred at reperfusion 1, 3, and 5 h after 1 h ischem ia-reperfusion lung injury, and the peak was on 3h after reperfusion. The apoptotic cells decreased in TMP groups compared with IR groups. The values of IQA in IR group were significantly higher than those in TMP group (P <0.01). There was a significant positive correlation between the apoptosis index and IQA (r = 0.718, P < 0.01). CONCLUSION: The apoptosis may significantly contribute to ischemia-reperfusion pulmonary injury and the tertram ethylpyrazine can protect PIRI by anti- apoptosis of pneumocytes.

Key words: pulmonary ischemia-reperfusion injury, the index of quantitative assessment of histologic lung (IQA), apoptosis, tertram ethylpyrazine

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