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缺血后处理对供体犬肺组织细胞凋亡基因表达的影响

鲁建军 翁慧雯 马俊 顾勇 罗红鹤

中山大学学报(医学科学版)2013,Vol.34Issue(1):53-58,6.
中山大学学报(医学科学版)2013,Vol.34Issue(1):53-58,6.

缺血后处理对供体犬肺组织细胞凋亡基因表达的影响

Ischemic Postconditioning Ameliorates Cellular Apoptosis of Transplanted Canine Lung

鲁建军 1翁慧雯 1马俊 1顾勇 1罗红鹤1

作者信息

  • 1. 中山大学附属第一医院胸外科,广东广州510080
  • 折叠

摘要

Abstract

[Objective] Ischemia reperfusion (I/R) injury is still inevitable for lung transplantation and ischemic postconditioning (I-postC) may benefit the function of a grafted lung. We investigated the influence of I-postC on expression of the apoptosis gene of canine donor lungs and observed the histomorphological changes under optical microscope. [Methods] Single left-lung orthotopic transplantation (LTx) was performed on 12 pairs of donor-and-recipient matched Beagle dogs. They were randomly subjected into an ischemic postconditioning (I-postC) group (n= 6) or a control group (n= 6). The transplantation procedure in control group was performed routinely, while I-postC protocol was added in the early stage of reperfusion for the experimental group: 10 seconds of reperfusion followed by 10 seconds of blockade, repeated three times. Expression of apoptosis gene Bcl-2 and Bax were measured by reverse transcription polymerase chain reaction (RT-PCR). Pathological changes of the donor lung were observed under an optical microscope. [Results] Compared with the experimental group, expression of Bcl-2 protein was up-regulated while expression of Bax protein was down-regulated. Observed under optical microscope, pulmonary inflammatory reaction was more moderate in I-postC group. [Conclusions] I-postC can attenuate the damage of ischemia-reperfusion injury. I-postC may affect the endogenous pathway of apoptosis by inhibiting expression of Bax and enhancing expression of Bcl-2.

关键词

啼移植/缺血后处理/缺血再灌注损伤/细胞凋亡基因

Key words

lung transplantation/ ischemic postconditioning/ ischemic reperfusion injury/ cellular apoptosis gene

分类

医药卫生

引用本文复制引用

鲁建军,翁慧雯,马俊,顾勇,罗红鹤..缺血后处理对供体犬肺组织细胞凋亡基因表达的影响[J].中山大学学报(医学科学版),2013,34(1):53-58,6.

基金项目

广东省自然科学基金博士启动项目(9451008901002331) (9451008901002331)

中山大学学报(医学科学版)

OA北大核心CSCDCSTPCD

1672-3554

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