Heme oxygenase-1 overexpression protects rat hearts from cold ischemia/reperfusion injury via an antiapoptotic pathway
Heme oxygenase-1 overexpression protects rat hearts from cold ischemia/reperfusion injury via an antiapoptotic pathway
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DOI：
10.1097/00007890-200201270-00023
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发表时间：
2002-01-27
期刊：
影响因子：
6.2
通讯作者：
Kupiec-Weglinski, JW
中科院分区：
文献类型：
--
作者：
Katori, M;Buelow, R;Kupiec-Weglinski, JW
背景缺血/再灌注（I/R）损伤是导致移植物早期丢失的重要原因之一。我们已经证明，血红素加氧酶-1（HO-1），一种诱导型热休克蛋白32的过度表达，可以保护大鼠肝脏免受I/R损伤。本研究以钴原卟啉（CoPP）为HO-1诱导剂，锌原卟啉（ZnPP）为HO-1受体，观察HO-1对大鼠心肌I/R损伤的细胞保护作用。研究了三组刘易斯大鼠：第1组对照供体在收获前48小时接受磷酸盐缓冲盐水;第2组供体在-48小时用CoPP预处理;以及在第3组中，供体在-48小时接受CoPP并且在再灌注时给予受体ZnPP。收集心脏，在威斯康星州大学溶液（4 ℃）中保存24小时，然后移植到同系（刘易斯）大鼠。60%的对照移植物在移植后停止了功能。
Background. Ischemia/reperfusion (I/R) injury is one of the most important causes of the early graft loss. We have shown that overexpression of heme oxygenase-1 (HO-1), an inducible heat shock protein 32, protects rat livers against I/R injury. We report on the cytoprotective effects of HO-1 in a rat cardiac I/R injury model, using cobalt protoporphyrin (CoPP) as HO-1 inducer and zinc protoporphyrin (ZnPP) as HO-1 inhibitor.Methods. Three groups of Lewis rats were studied: group 1 control donors received phosphate-buffered saline 48 hr before the harvest; group 2 donors were pretreated with CoPP at -48 hr; and in group 3, donors received CoPP at -48 hr and ZnPP was given to recipients at reperfusion. Hearts were harvested, stored in University of Wisconsin solution (4degreesC) for 24 hr, and then transplanted to syngeneic (Lewis) rats.Results. Sixty percent of control grafts ceased their function in