牛磺酸对甲状腺激素致血管内皮细胞损伤的保护作用及机制

Protective effects of taurine on thyroid hormone-induced vascular endothelial cell injury and its mechanism

目的探讨牛磺酸(taurine)对甲状腺激素(thyroid hormone,TH)致血管内皮细胞损伤的保护作用及其机制。方法在体外培养的人脐静脉血管内皮细胞(human umbilical vein endothelial cells,HUVECs)中,MTT法检测细胞存活率;流式细胞技术检测HUVECs内活性氧(ROS)水平;硝酸还原酶法检测细胞培养液中的一氧化氮(NO)水平。结果体外培养的HUVECs实验结果显示,L-四碘甲状腺原氨酸(T4)诱导细胞存活率的降低和胞内ROS的升高,而牛磺酸干预则明显抑制此种变化;T4降低细胞培养液中NO水平,而牛磺酸干预则明显抑制T4致NO水平降低效应;用PI3K/Akt阻断剂wortmanin预处理HUVECs后,牛磺酸抑制T4致NO水平降低效应则消失。结论牛磺酸对TH致血管内皮细胞损伤具有保护作用,其机制与PI3K/Akt-eNOS-NO信号通路有关。

Objective:To investigate the protective effects and underlying mechanism of taurine on thyroid hormone(TH)-induced vascular endothelial cell injury.Methods:Human umbilical vein endothelial cells(HUVECs)were cultured in vitro.Methyl thiazolyl tetrazolium assay(MTT),flow cytometry and nitrate reductase were used in this study.Results:T4 decreased cell viability and increased the production of reactive oxygen species(ROS)in HUVECs.Taurine inhibited T4-induced decrease in cell viability and increase in the production of ROS in HUVECs.T4 decreased the levels of nitric oxide(NO)in the cell culture supernate from HUVECs.Wortmanin,a PI3K/Akt inhibitor,and abolished the reserve effect of taurine on T4-induced decrease in the levels of NO in HUVECs.Conclusion:These results demonstrate that taurine can protect TH-induced vascular endothelial injury,which is related to the PI3K/Akt-eNOS-NO signaling.