同型半胱氨酸对心肌细胞的损伤作用及其信号转导机制探讨

被引:12
作者
吴淑庆
弓景波
陈良恩
钱令嘉
机构
[1] 军事医学科学院卫生学环境医学研究所,军事医学科学院卫生学环境医学研究所,军事医学科学院卫生学环境医学研究所,军事医学科学院卫生学环境医学研究所天津,天津,天津,天津
关键词
同型半胱氨酸; 心肌细胞; 信号转导;
D O I
10.13459/j.cnki.cjap.2003.01.009
中图分类号
R540.2 [];
学科分类号
摘要
目的 :观察同型半胱氨酸 (homocysteine ,HCY)对心肌细胞的损伤作用 ,探讨该作用发生的信号转导机制及其关键调控环节。方法 :分离培养Wistar乳鼠心肌细胞 ,经HCY作用后 ,以台盼蓝排斥实验测定细胞存活率 ,TUNEL法和流式细胞仪测定细胞凋亡率 ,免疫印迹法测定心肌细胞ERK2蛋白磷酸化水平 ,阻滞电泳法测定细胞NF κB活化水平。结果 :作用后 ,心肌细胞存活率显著降低 ,存活率降低程度与HCY的作用浓度、作用时间具有明确的剂量 效应关系及时间 效应关系 ;在 1 0 - 3mol/LHCY作用下 ,心肌细胞凋亡率升高 ,于 4h达峰值 ,为 7.56 % ;1 0 - 3、1 0 - 4、1 0 - 5mol/LHCY均可抑制心肌细胞ERK2磷酸化 ,其中 1 0 - 3mol/LHCY作用于心肌细胞后 ,ERK2蛋白磷酸化水平呈现迅速而明显的降低 ,4h降至对照组的 3 .0 4 % (P <0 .0 1 ) ;不同浓度HCY均明显阻抑NF κB的活化。结论 :HCY具有明显心肌细胞损伤作用 ,对心肌细胞凋亡的诱导是HCY心肌细胞损伤作用的形式之一 ;HCY可影响心肌细胞信号转导通路ERK ,并通过对转录因子NF κB的活化抑制 ,导致心肌细胞损伤
引用
收藏
页码:26 / 30+106
页数:6
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