The protective role of 5-HMF against hypoxic injury
The protective role of 5-HMF against hypoxic injury
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5-HMF对缺氧损伤的保护作用
DOI：
10.1007/s12192-010-0238-2
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发表时间：
2011-05-01
影响因子：
3.8
通讯作者：
Fan, Ming
中科院分区：
文献类型：
--
作者：
Li, Ming-Ming;Wu, Li-Ying;Fan, Ming
为了从草药中寻找新型的抗缺氧剂，我们鉴定了5-羟甲基-2-糠醛（5-HMF）作为满足标准的天然试剂。5-HMF是碳水化合物代谢的最终产物，具有良好的生物学作用，如抗氧化活性和抑制红细胞镰状化。然而，5-HMF在缺氧中的作用尚不清楚。我们的初步研究结果表明，5-HMF预处理明显增加了小鼠在缺氧应激下的存活时间和存活率。本研究以ECV 304细胞为模型，探讨5-HMF对缺氧损伤的保护作用及其机制。用5-HMF预处理ECV 304细胞1h，观察缺氧（0.3%O-2）24 h后细胞凋亡、坏死、线粒体膜电位（MMP）和磷酸化细胞外信号调节激酶（p-ERK）表达的变化。5-HMF预处理可明显减轻缺氧晚期细胞坏死和凋亡（p < 0.01）。5-HMF预处理可逆转缺氧条件下MMP的下降和p-ERK蛋白的升高。上述结果提示，5-HMF对ECV 304细胞缺氧损伤具有保护作用，其机制可能与其对MMP和p-ERK的影响有关。
In an attempt to find new types of anti-hypoxic agents from herbs, we identified 5-hydroxymethyl-2-furfural (5-HMF) as a natural agent that fulfills the criterion. 5-HMF, the final product of carbohydrate metabolism, has favorable biological effects such as anti-oxidant activity and inhibiting sickling of red blood cells. The role of 5-HMF in hypoxia, however, is not yet. Our pilot results showed that pretreatment with 5-HMF markedly increased both the survival time and the survival rate of mice under hypoxic stress. The present study was aimed to further investigate the protective role of 5-HMF and the underlying mechanisms in hypoxic injury using ECV304 cells as an in vitro model. ECV304 cells pretreated with or without 5-HMF for 1 h were exposed to hypoxic condition (0.3% O-2) for 24 h and then cell apoptosis, necrosis, the changes of mitochondrial membrane potential (MMP) and the expressions of phosphorylation- extracellular signal-regulated kinase (p-ERK) were investigated. Pretreatment with 5-HMF markedly attenuated hypoxia-induced cell necrosis and apoptosis at late stage (p < 0.01). Furthermore, pretreatment with 5-HMF rescued both the decline of the MMP and the increase of p-ERK protein under hypoxia. In a word, these results indicated that 5-HMF had protective effects against hypoxic injury in ECV304 cells, and its effects on MMP and p-ERK may be involved in the mechanism.