Hydrogen Sulfide-Induced Hypometabolism Prevents Renal Ischemia/Reperfusion Injury
Hydrogen Sulfide-Induced Hypometabolism Prevents Renal Ischemia/Reperfusion Injury
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DOI：
10.1681/asn.2008121269
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发表时间：
2009-09-01
影响因子：
13.6
通讯作者：
van Goor, Harry
中科院分区：
文献类型：
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作者：
Bos, Eelke M.;Leuvenink, Henri G. D.;van Goor, Harry
硫化氢(H(2)S)在亚毒性浓度下可诱导哺乳动物进入低代谢、类冬眠状态。从药物上减少对氧气的需求是减少肾移植过程中不可避免的缺氧损伤，如缺血/再灌注损伤的一种有前景的策略。在这里，我们证明了H(2)S降低了体内、体外和体外的新陈代谢。此外，我们还用三种不同的治疗策略证明了H(2)S诱导的低代谢在双侧肾缺血/再灌注损伤模型中的有益作用。结果表明，对存活、肾功能、细胞凋亡和炎症有显著的保护作用。H(2)S诱导的低代谢状态可能对缺氧肾脏有保护作用。
Hydrogen sulfide (H(2)S) can induce a hypometabolic, hibernation-like state in mammals when given in subtoxic concentrations. Pharmacologically reducing the demand for oxygen is a promising strategy to minimize unavoidable hypoxia-induced injury such as ischemia/reperfusion injury during renal transplantation. Here we show that H(2)S reduces metabolism in vivo, ex vivo, and in vitro. Furthermore, we demonstrate the beneficial effects of H(2)S-induced hypometabolism in a model of bilateral renal ischemia/reperfusion injury using three different treatment strategies. The results demonstrate striking protective effects on survival, renal function, apoptosis, and inflammation. A hypometabolic state induced by H(2)S might have therapeutic potential to protect kidneys that suffer from hypoxia.