氯化高铁血红素对血管内皮细胞Erk1/2磷酸化的诱导及维持作用研究

Hemin induces and sustains the phosphorylation of Erk1/2 in human umbilical vascular endothelial cells

目的:探讨氯化高铁血红素(hemin)是否可诱导人脐静脉内皮细胞Erk1/2的磷酸化,以及对磷酸化Erk1/2的维持时间。方法:人脐静脉内皮细胞(HUVECs)分别给予不同浓度的氯化高铁血红素或100μmol/L H2O2刺激,收集不同时段的细胞,采用Western blotting测定细胞中总Erk1/2和磷酸化Erk1/2的表达。结果:氯化高铁血红素在1-10μmol/L浓度范围内可诱导HUVECs Erk1/2的磷酸化,且可长时间维持Erk1/2的磷酸化,然而当氯化高铁血红素浓度≥25μmol/L时,对HUVECs Erk1/2的磷酸化作用减弱甚至消失。H2O2对照组作用于HUVECs时仅引起Erk1/2短暂的磷酸化。结论:氯化高铁血红素可诱导并维持HUVECs Erk1/2长时间的磷酸化,提示对Erk1/2的磷酸化可能是氯化高铁血红素的作用机制之一。

AIM： To investigate the relationship between hemin and Erk1/2 activation in human umbilical vascular endothelial cells （HUVECs）. METHODS： Cultured HUVECs were separately incubated with hemin or H2O2 for different times. Subsequently Erk1/2 phosphorylation and total Erk1/2 were determined by Western blotting assay. Flow cytometry was employed to determine the cell cycle distribution. RESULTS： Hemin at the concentration of 1 - 10 μmol/L induced the phosphorylation of Erk1/2 in HUVECs, and sustained the phosphorylation of Erk1/2 for three hours. The duration of phospho-Erk1/2 induced by hemin was much longer than that in H2O2 control （3 h vs 30 min）. CONCLUSION： Hemin induces and sustains the phosphorylation of Erk1/2 in HUVECs, which indicates that the effect of hemin on the Erk1/2 activation may be one of pharmacological target of hemin.