Heat shock provides delayed protection against oxidative injury in cultured human umbilical vein endothelial cells
Heat shock provides delayed protection against oxidative injury in cultured human umbilical vein endothelial cells
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DOI：
10.1006/jmcc.1998.0837
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发表时间：
1998-12-01
影响因子：
5
通讯作者：
Sholley, MM
中科院分区：
文献类型：
--
作者：
Gill, RR;Gbur, CJ;Sholley, MM
在轻度和重度缺血期间，缺血器官的大血管和小血管内衬的血管内皮细胞暴露于氧衍生的自由基，导致对器官的氧化损伤。热休克预处理可诱导内皮细胞产生热耐受，并可能通过增加热休克蛋白（HSP）的合成而保护内皮细胞免受缺血性损伤。对培养的人脐静脉内皮细胞（HUVEC）进行热休克（42 ℃，1小时），并使其恢复2或20小时，此时通过将细胞暴露于100-200 μ mol/l的过氧化氢（H2 O2）而使细胞氧化应激1小时。通过形态学和乳酸脱氢酶（LDH）释放来评估即刻和18 h后的细胞损伤。使用2小时恢复间隔没有观察到HUVEC的保护作用，但有显著的保护作用（P
During both mild and severe ischemia, vascular endothelial cells lining large and small vessels of the ischemic organ are exposed to oxygen-derived free radicals resulting in oxidative damage to the organ. Heat shock has been shown to induce thermotolerance and also protect against ischemic injury, possibly via increased synthesis of heat shock proteins (HSPs), We hypothesized that heat shock preconditioning may protect human endothelial cells against oxidative damage. Cultured human umbilical Vein endothelial cells (HUVEC) were subjected to heat shock (42 degrees C, Ih) and allowed to recover for 2 or 20 h, at which times the cells were oxidatively stressed for Ih by exposing them to 100-200 mu mol/l of hydrogen peroxide (H2O2). Cellular damage was assessed immediately and 18 h later by morphology and release of lactate dehydrogenase (LDH). No protection of HUVEC was seen using the 2-hour recovery interval, but a significant protection (P