在心脏全移植中,介导的降低了细胞亡
M H Kown1, T Van der Steenhoven, F G Blankenberg
1Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305-5247, USA.
Circulation
|November 18, 2000
概括
化 (ZnCl2) 通过抑制caspase-3活性,有效地减少急性心脏全移植排斥期间的亡. 这项研究表明,在接受治疗的老鼠中,剂量依赖的亡减少,并改善了移植的存活率.
科学领域:
- 免疫学 免疫学 免疫学
- 移植生物学 移植生物学
- 生物化学 生物化学
背景情况:
- 免疫媒介性急性拒绝心脏异位移植涉及亡.
- 实验室研究表明,可以抑制前性酶caspase-3.
- 这项研究研究化 (ZnCl2) 作为一种潜在的治疗药物来阻断体内卡斯帕-3依赖性亡.
研究的目的:
- 为了评估ZnCl2在急性心脏异位移植排斥期间减少亡的疗效.
- 为了确定ZnCl2的使用是否会影响移植的存活率.
- 评估ZnCl2对心脏全移植中的caspase-3活性的影响.
主要方法:
- 在大鼠模型中进行异型心脏移植 (PVG到ACI).
- 给受试大鼠使用不同剂量的ZnCl2 (1和5mg/kg) 或盐水.
- (99m) 标记Tc的附录V成像,以量化全移植中的亡.
- 测量移植的存活时间和caspase-3活性.
主要成果:
- 治疗ZnCl2导致 (99m) Tc附件V吸收的剂量依赖性减少,这表明亡减少.
- 与对照组相比,在用ZnCl2治疗的老鼠中,移植存活时间明显延长.
- 在高剂量ZnCl2组中,所有移植中的caspase-3活性显著降低.
结论:
- ZnCl2有效地减少了急性心脏异位移植排斥中的亡.
- 观察到的亡减少是通过抑制caspase-3的介导.
- ZnCl2证明了治疗心脏异位移植排斥的治疗潜力.
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