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糖尿病大鼠心肌磷酸受纳蛋白基因表达和肌浆网Ca2+-ATPase活性的变化
Alterations of phospholamban expression and cardiac sarcoplasmic reticulum Ca ~(2+)-ATPase activity in diabetic rats
【摘要】 目的:观察糖尿病(DM)大鼠心肌磷酸受纳蛋白(PLB)基因表达和肌浆网Ca2+-ATPase活性的变化及其与心功能的关系。方法:复制糖尿病大鼠模型,分别于4、6、8周后对糖尿病组和对照组进行左心室血流动力学检测,测定心肌PLBmRNA转录水平以及蛋白表达水平变化,检测心肌肌浆网Ca2+-ATPase活性。结果:糖尿病大鼠心肌PLBmRNA转录和蛋白表达水平4周时与正常大鼠无明显差异,6周时和8周时明显高于正常大鼠;肌浆网Ca2+-ATPase活性4周时无明显改变,6周时和8周时明显低于正常大鼠;糖尿病大鼠4周时LVSP、LVEDP、±dp/dtmax与正常大鼠无明显差异,6周、8周时LVSP、±dp/dtmax显著降低,LVEDP显著升高。结论:糖尿病大鼠心肌PLB表达水平升高,肌浆网Ca2+-ATPase活性降低,引起心功能下降。
【Abstract】 AIM:To investigate the alterations of phospholamban(PLB)expression and cardiac sarcoplasmic reticulum(SR)Ca 2+-ATPase activity,and the change of cardiac function in rats with diabetes mellitus(DM).METHODS:The diabetes mellitus in male Wistar rats was induced by intraperitoneal injection of streptozotocin.The levels of PLB mRNA and PLB protein,the activity of SR Ca 2+-ATPase and the left ventricular hemodynamics parameters were measured 4 weeks,6 weeks and 8 weeks after DM was induced in rats,while the normal rats served as control group.RESULTS:There was no significant difference in PLB mRNA level and protein level between 4-week-DM rats and normal control rats.6-week-DM rats and 8-week-DM rats had markedly increased PLB mRNA and protein level compared with normal control rats.SR Ca 2+-ATPase activity was not significantly changed in 4-week-DM rats compared with normal control rats,and was markedly depressed in 6-week-DM rats and 8-week-DM rats.LVSP,LVEDP and ±dp/dt max were not significantly changed in 4-week-DM rats compared with normal control rats.In 6-week-DM rats and 8-week-DM rats,LVSP and ±dp/dt max were decreased,LVEDP was increased compared with normal control rats.CONCLUSION:The elevated levels of PLB mRNA and PLB protein contribute to SR Ca 2+-ATPase activity reduction,which leads to cardiac dysfunction in DM rats.
【Key words】 Diabetes mellitus; Phospholamban; Sarcoplasmic reticulum; Ca 2+-ATPase; Gene expression;
- 【文献出处】 中国病理生理杂志 ,Chinese Journal of Pathophysiology , 编辑部邮箱 ,2006年09期
- 【分类号】R587.1
- 【被引频次】5
- 【下载频次】112