甲状腺激素类似物和白三烯通路阻滞剂对心脏移植后再灌注损伤衰减的影响。

ISRN Pharmacology Pub Date : 2013-09-17 eCollection Date: 2013-01-01 DOI:10.1155/2013/303717
Fadhil G Al-Amran, Najah R Hadi, Haider S H Al-Qassam
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引用次数: 2

摘要

背景。心脏移植后全身心肌缺血再灌注损伤被认为会损害移植物功能,加重急性和慢性排斥反应。目标。探讨MK-886和3,5-二碘甲状腺丙酸DITPA对心脏移植术后心肌缺血再灌注损伤的保护作用。材料与方法。将成年白化病大鼠随机分为6组:1组假手术组;第二组为对照组;第三组和第四组为对照车辆(1,2);V组,MK-886处理组。供鼠在移植前30分钟给予MK-886,受体再灌注时重复相同剂量;第六组,即DITPA治疗组,供鼠和受体大鼠在移植前接受DITPA预处理7 d。结果。MK-886和DITPA均能显著抑制心肌TNF- α、IL-1 β、ICAM-1水平升高及血浆cTnI水平升高(P < 0.05)。形态学分析表明,MK-886和DITPA均能显著改善异位移植大鼠心脏损伤的严重程度(P < 0.05)。结论。我们的研究结果表明,MK-886和DITPA都可能通过干扰炎症通路改善心脏移植术后全身心肌缺血再灌注损伤。
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Effects of thyroid hormone analogue and a leukotrienes pathway-blocker on reperfusion injury attenuation after heart transplantation.

Background. Global myocardial ischemia reperfusion injury after heart transplantation is believed to impair graft function and aggravate both acute and chronic rejection episodes. Objectives. To assess the possible protective potential of MK-886 and 3,5-diiodothyropropionic acid DITPA against global myocardial ischemia reperfusion injury after heart transplantation. Materials and Methods. Adult albino rats were randomized into 6 groups as follows: group I sham group; group II, control group; groups III and IV, control vehicles (1,2); group V, MK-886 treated group. Donor rats received MK-886 30 min before transplantation, and the same dose was repeated for recipients upon reperfusion; in group VI, DITPA treated group, donors and recipients rats were pretreated with DITPA for 7 days before transplantation. Results. Both MK-886 and DITPA significantly counteract the increase in the levels of cardiac TNF- α , IL-1 β , and ICAM-1 and plasma level of cTnI (P < 0.05). Morphologic analysis showed that both MK-886 and DITPA markedly improved (P < 0.05) the severity of cardiac injury in the heterotopically transplanted rats. Conclusions. The results of our study reveal that both MK-886 and DITPA may ameliorate global myocardial ischemia reperfusion injury after heart transplantation via interfering with inflammatory pathway.

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