【摘要】 目的探讨锌及锌转运体Zip13在高盐诱导的左心室舒张功能障碍(LVDD)大鼠心肌中的表达及作用机制。方法将36只Dahl盐敏感大鼠(Dahl salt-sensitive rat,DSS大鼠)随机分为模型组(8%氯化钠高盐饮食,n=22)和对照组(0.3%氯化钠饮食,n=14)。用Vevo 2100小动物超声仪评价各组大鼠心功能;电感耦合等离子体发射光谱法(inductively coupled plasma optical emission spectroscopy, ICP-DES)测定血清和心肌组织中锌离子浓度;分别用Western blot和荧光实时定量PCR技术检测心肌中Zip13的蛋白和mRNA表达水平。结果与对照组相比,模型组左心室后壁舒张末期厚度(LVPWd)、左心室舒张末期内径(LVDd)、舒张末期室间隔厚度(IVSd)、左心室后壁收缩末期厚度(LVPWs)、左心室质量(LVM)以及左心室体重比(LVM/Weight)均显著升高(P<0.05)。心肌组织中锌离子浓度明显升高,而血清中锌离子浓度明显降低(P<0.05);模型组心肌组织中Zip13蛋白和mRNA表达水平均显著升高(P<0.05)。结论 LVDD大鼠出现了心肌锌离子浓度升高的锌稳态失衡,同时Zip13蛋白和mRNA表达均上调,提示Zip13可能参与了调控和纠正锌稳态失衡,从而实现抑制LVDD心肌重构作用,具体机制有待进一步研究。更多还原

【Abstract】 Objective To investigate the expressions and mechanisms of zinc and zinc transporter(Zip13) in the myocardium of rats with hypersalt-induced left ventricular diastolic dysfunction(LVDD). Methods A total of 36 Dahl salt-sensitive(DSS) rats were randomly divided into model group(a high-salt diet containing 8% NaCl, n=22) and control group(a high-salt diet containing 0.3% NaCl, n=14). The Vevo 2100 ultrasound equipment for small animals was used to evaluate the cardiac function of rats in each group. The concentrations of zinc ions in serum and myocardial tissues were determined by inductively coupled plasma optical emission spectroscopy(ICP-DES). The protein and mRNA expressions of Zip13 in the myocardium were detected by Western blot and RT q-PCR methods. Results Compared with the control group, the model group showed significant increase in left ventricular posterior wall at end-diastole(LVPWd), left ventricular end-diastolic dimension(LVDd), left ventricular end systolic dimension(LVSd), left ventricular posterior wall at end-systole(LVPWs), left ventricular mass(LVM) and ratio of LVM to weight(LVM/weight)(P<0.05). The concentration of zinc ions in myocardial tissues significantly increased, while that in serum decreased obviously(P<0.05). The expressions of Zip13 protein and mRNA in myocardial tissues of the model group significantly increased(P<0.05).Conclusion LVDD rats had a zinc homeostasis with elevated myocardial zinc ion concentration. And the expressions of Zip13 protein and mRNA were up-regulated, which indicated that Zip 13 may help regulate and correct the zinc homeostasis and inhibited myocardial remodeling of LVDD. The specific mechanism needs to be further studied.更多还原