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急性心肌缺血大鼠肺组织肿瘤坏死因子-α及mRNA表达的研究
引用本文:周日华,王晋平,郭政. 急性心肌缺血大鼠肺组织肿瘤坏死因子-α及mRNA表达的研究[J]. 中国药物与临床, 2008, 8(5): 344-347
作者姓名:周日华  王晋平  郭政
作者单位:山西医科大学第二医院麻醉科,太原030001
摘    要:目的观察急性心肌缺血大鼠肺组织中肿瘤坏死因子-α(TNF-α)及TNF-αmRNA的表达,探讨TNF-α及TNF-αmRNA在急性心肌缺血诱发肺损伤中的作用。方法健康成年雄性SD大鼠36只,体质量(250±20)g,随机分为两组:手术对照组(S组)和结扎冠状动脉缺血组(CAO组)。S组动物仅开胸但不结扎冠状动脉左前降支;CAO组动物开胸后结扎冠状动脉左前降支。S组、CAO组又各分为1、3、6 h三个不同的时点组。各组在开胸或扎闭冠状动脉左前降支后分别计时1 h,3 h,6 h取出右肺下叶。采用免疫组织化学、原位杂交两种方法观察TNF-α及TNF-αmRNA在各组动物肺组织中的表达情况。结果CAO组各时间点大鼠的支气管上皮细胞、肺泡Ⅱ型细胞和血管内皮细胞均可见到TNF-α及TNF-αmRNA的均呈强阳性表达(P<0.01),在3 h达高峰。结论TNF-α及TNF-αmRNA参与了急性心肌缺血诱发肺损伤的发生和发展。

关 键 词:急性心肌缺血  肿瘤坏死因子-α  信使RNA
修稿时间:2008-02-22

Expressions of TNF-α and its mRNA in lung tissue of rats with coronary artery occlusion
ZHOU Ri-hua,WANG Jin-ping,GUO Zheng. Expressions of TNF-α and its mRNA in lung tissue of rats with coronary artery occlusion[J]. Chinese Remedies & Clinics, 2008, 8(5): 344-347
Authors:ZHOU Ri-hua  WANG Jin-ping  GUO Zheng
Affiliation:( Department of Anesthesiology, the Second Hospital of Shanxi Medical University, Taiyuan 030001, China )
Abstract:Objective To investigate the expressions of TNF-α and its mRNA in rat lungs following coronary artery occlusion (CAO) and to explore the effects of TNF-α and its mRNA in CAO-induced lung injury. Methods Thirty-six adult male Sprague-Dawley rats [(250±20)g in weight] were randomized into two groups (n=6 each): the sham surgery group (group S) and the CAO group. Thoracotomy was performed in all rats and the left anterior descending branch of coronary artery was occluded in the CAO group but not in group S. The two groups were further stratified by 1 h, 3 h and 6 h from thoracotomy to form subgroups S1 h, S3 h, S6 h, CAO1 h, CAO3 h and CAO6 h. The rats were harvested for inferior lobe of right lung at 1 h, 3 h or 6 h, according to the subgroup-related timetable. Expressions of TNF-α and its mRNA in lung tissue were studied using immunohistochemistry and in-situ hybridization. Results In all time-related CAO groups, strong expressions of TNF-α and its mRNA were shown in bronchial epithelium, type 2 pneumocytes and vascular endothelium (P〈0.01), with highest levels at 3 h. Conclusion TNF-α protein and its mRNA may have a role in the formation and progression of CAO-induced lung injury.
Keywords:Acute myocardial ischemia  Tumor necrosis factor-α  mRNA
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