甲状旁腺素对大鼠心肌细胞内游离钙和细胞凋亡的影响

目的　研究甲状旁腺素 (PTH)对心肌细胞内游离钙以及细胞肥大和凋亡的影响。方法　利用培养的新生大鼠心肌细胞 ,以Fluo 3/AM负载 ,通过激光共聚焦显微镜(LSCM)测定细胞内游离钙浓度 (Ca2 + ] i) ;以细胞面积和细胞蛋白含量作为心肌细胞肥大指标 ;采用电镜和流式细胞术观察细胞凋亡的变化。结果　PTH1～ 34 0 0 1和 0 1 μmol·L- 1 刺激 7d后 ,心肌细胞内钙荧光强度以及心肌细胞面积和蛋白含量、细胞凋亡率较对照组显著增加。而 0 1 μmol·L- 1 PTH1～ 34 刺激的同时分别加入 1、1 0 μmol·L- 1 硝苯地平 ,上述指标改善 ,但未能达正常。结论　PTH1～ 34 可显著增加心肌细胞 Ca2 + ] i,诱导细胞肥大和凋亡 ,并呈浓度依赖性 ,电压依赖性钙通道开放引起的细胞外钙内流增加为其机制之一

The effects of parathyroid hormone on intracellular[Ca2+]i and apoptosis in rat cardiomyocytes

AIM To study the effects of parathyroid hormone(PTH) on intracellular calcium concentration(Ca 2+ ] i), hypertrophy and apoptosis in rat cardiomyocytes. METHODS Neonatal rat cardiomyocyte hypertrophic response was assayed by measuring cell surface area and protein content. Ca 2+ ] i was measured by confocal microscope using Fluo 3/AM as fluorescent indicator.Apoptosis was determined by flow cytometer and electron microscope. RESULTS After 7 d exposure to PTH 1～34 of 0 01 and 0 1 μmol·L -1 ,Ca 2+ ] i,surface area and protein content,and apoptosis rate(APO) of cardiomyocytes were significantly increased,especially in high concentration groups. While application of both nifedipine and PTH 1～34 significantly decreased lose indicators, they were still markedly higher than normal. CONCLUSIONS PTH 1～34 dose dependently induces hypertrophy and apoptosis of cardiomyocyte,and this is attributed able to augmented entry of calcium into cell via voltage dependent Ca 2+ channel.