论文部分内容阅读
目的:观察牛磺酸(Tau)对舒张性心力衰竭(DHF)大鼠心肌细胞内钙离子浓度[Ca2+]i和心肌细胞膜上ATP酶活性的影响。方法:采用腹主动脉缩窄法建立DHF模型,术后4周随机分为模型组,Tau高、中、低剂量组(400,200,100 mg.kg-1.d-1)4组(n=10),另有假手术组10只。连续给药4周,酶解法分离DHF大鼠心肌细胞,以Fluo-3AM荧光指示剂负载,应用激光扫描共聚焦显微镜(LSCM)技术检测心肌细胞内[Ca2+]i变化,[Ca2+]i用荧光强度(FI)表示;通过ATP酶试剂盒,采用酶促反应定磷比色法测定心肌细胞膜上ATP酶活性。结果:与假手术组相比,模型组大鼠心肌细胞内Ca2+浓度明显上升,心肌细胞膜上ATP酶活性明显下降。与模型组比较,Tau高剂量组显著降低心肌细胞内荧光值,明显升高ATP酶活性;Tau中剂量组明显降低心肌细胞内荧光值和ATP酶活性;Tau低剂量组明显升高心肌细胞内荧光值,显著降低ATP酶活性。结论:大剂量的Tau可以明显提高DHF大鼠心肌细胞膜ATP酶活性,改善DHF大鼠心肌细胞内[Ca2+]i,拮抗钙超载。
Objective: To observe the effects of taurine (Tau) on intracellular calcium concentration [Ca2+]i and ATPase activity on myocardium membrane in rats with dilated heart failure (DHF). METHODS: DHF models were established by abdominal aortic coarctation. They were randomly divided into model groups 4 weeks after surgery and 4 groups (400, 200, 100 mg.kg-1.d-1) of Tau high, middle and low doses (n=10). There were 10 other sham groups. After continuous administration for 4 weeks, DHF rat cardiomyocytes were isolated by enzymolysis and loaded with Fluo-3AM fluorescent indicator. The changes of [Ca2+]i in myocardial cells were detected by laser scanning confocal microscopy (LSCM) technique, and [Ca2+]i was used as fluorescence. Intensity (FI) is indicated; the ATPase activity on the myocardial cell membrane was measured by the enzyme-promoted phosphor-fixing assay using the ATPase kit. RESULTS: Compared with the sham-operated group, the myocardial Ca2+ concentration in the model group increased significantly, and the ATPase activity in the myocardial cell membrane was significantly decreased. Compared with the model group, Tau high dose group significantly decreased the intracellular fluorescence value, significantly increased ATPase activity; Tau medium dose group significantly reduced myocardial intracellular fluorescence and ATPase activity; Tau low dose group significantly increased myocardial cell The fluorescence value significantly reduced ATPase activity. Conclusion: High-dose Tau can significantly increase ATPase activity of myocardial cell membrane in DHF rats, improve [Ca2+]i in myocardial cells of DHF rats, and antagonize calcium overload.