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在心脏异位移植排斥期间COX-2的升级
1Departments of Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
Circulation
|February 2, 2000
概括
循环氧化原酶-2 (COX-2) 和可诱导的氧化合成酶 (iNOS) 在心脏全移植排斥中被上调. 抑制COX-2和iNOS适度增加了全移植存活率,但没有显著降低排斥强度或肌细胞亡.
科学领域:
- 免疫学 免疫学 免疫学
- 心血管研究研究心血管研究
- 药理学 药理学是指药理学的学科.
背景情况:
- 调查循环氧化酶-2 (COX-2) 在心肌炎炎症中的作用.
- 使用大鼠异型腹部心脏移植模型.
研究的目的:
- 为了确定COX-2在心脏异位移植排斥的炎症反应中的参与.
- 评估COX-2和诱导性氧化合成酶 (iNOS) 抑制对全移植存活率和排斥标志物的影响.
主要方法:
- 在拒绝心脏全移植时,对COX-2和iNOS mRNA和蛋白质表达的量化.
- 对COX-2局部化的免疫组织化学分析.
- 测量前列腺素 (PG) 水平.
- 选择性COX-2和iNOS抑制剂的使用,以评估其作用.
- 评估全移植存活率,肌细胞亡 (TUNNEL试验) 和排斥强度.
主要成果:
- 与综合基因对照相比,COX-2和iNOS在拒绝心脏异位移植方面显著上调.
- 在透的巨细胞和受损的心脏肌细胞中局部化了COX-2.
- 在拒绝全移植时,前列腺素水平升高.
- 抑制剂治疗降低了COX-2 mRNA和iNOS活性,适度增加了全移植存活 (5.4至6.4天).
- 肌细胞亡和排斥强度仅受到抑制剂治疗的边际影响.
结论:
- 在心脏全移植排斥过程中,心肌中的COX-2表达与iNOS并行增强.
- 虽然COX-2和iNOS抑制显示出适度的生存益处,但它并不能完全缓解排斥过程或肌细胞损伤.
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