首页> 外文期刊>Nephron >Hyperthermia preconditioning induces renal heat shock protein expression, improves cold ischemia tolerance, kidney graft function and survival in rats.
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Hyperthermia preconditioning induces renal heat shock protein expression, improves cold ischemia tolerance, kidney graft function and survival in rats.

机译:热疗预处理可诱导肾热休克蛋白表达,提高大鼠的抗冷缺血性,移植肾功能和存活率。

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Background: Evidence indicates that hyperthermia preconditioning (HP) can be protective in kidney transplantation, possibly through increased heat shock protein (HSP) expression. A detailed study about individual HSPs and functional preservation is lacking, however. Therefore, we studied the effects of HP on kidney graft survival, function and HSP expression. Methods: Male Lewis rats were or were not subjected to whole-body hyperthermia 24 h prior to kidney procurement. Kidneys were stored in UW solution at 4 degrees C for 32, 40 or 45 h. Recipient kidneys were both removed and single isografts transplanted orthotopically. Results: HP strongly induced HSP72 and HSP32 expression. Following 32-hour cold ischemia, most animals survived even without prior HP. However, HP strongly reduced functional impairment induced by cold ischemia. Following 40-hour cold ischemia, kidneys from donors without HP did not recover function and all animals died within 3 days. In contrast, HP-exposed kidneys tolerated 40-hour storage significantly better, with 44% of rats surviving until sacrifice on day 7. In these animals, renal function was still better compared to animals with 32-hour-stored kidneys without HP. Histological alterations were also diminished following HP. Conclusion: Our data show that HP induces renal HSP72 and, for the first time, HSP32. HP increases survival following transplantation and acts by improving several parameters of kidney function including proteinuria, volume output and creatinine clearance.
机译:背景:有证据表明,高温预处理(HP)在肾脏移植中可能具有保护作用,可能是通过增加热休克蛋白(HSP)的表达来实现的。但是,缺少有关单个HSP和功能保存的详细研究。因此,我们研究了HP对肾移植物存活,功能和HSP表达的影响。方法:雄性Lewis大鼠在肾脏获取前24 h接受或不接受全身热疗。将肾脏在4摄氏度的UW溶液中保存32、40或45小时。取出接受者的肾脏并原位移植单个同种异体移植物。结果:HP强烈诱导HSP72和HSP32表达。经过32小时的冷缺血后,即使没有HP,大多数动物也可以存活。但是,HP强烈降低了冷缺血引起的功能障碍。在40小时的冷缺血后,没有HP的供体的肾脏无法恢复功能,所有动物在3天内死亡。相反,暴露于HP的肾脏耐受40小时的储存明显更好,其中44%的大鼠存活至第7天被处死为止。在这些动物中,与具有32小时储存的无HP肾脏的动物相比,肾功能仍然更好。 HP后组织学改变也减少了。结论:我们的数据表明HP诱导了肾脏HSP72,并且首次诱导了HSP32。 HP可提高移植后的存活率,并通过改善肾脏功能的多个参数(包括蛋白尿,血容量输出和肌酐清除率)发挥作用。

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