摘要
目的 :观察虎杖甙 (polydatin ,PD)对大鼠心肌细胞内游离钙浓度 ( [Ca2 +]i)的影响 ,以探讨PD增强心肌细胞收缩性的作用机制。方法 :用荧光染料Fluo- 3 -AM标记细胞 ,在粘附式细胞仪上测定细胞 [Ca2 +]i的变化。结果 :给予PD后心肌 [Ca2 +]i升高。但不同细胞群的 [Ca2 +]i升幅不一致。 10min后有些细胞 [Ca2 +]i仅升至起始浓度的 111 80 %± 2 2 2 %,有些细胞内钙则急升到最初的 2 2 4 0 0 %± 2 4 3 3 %。当先用EGTA或维拉帕米分别预孵育10min后再加PD ,细胞 [Ca2 +]i则呈持续下降趋势 ,10min后 [Ca2 +]i下降至起始浓度的 5 3 0 0 %± 9 2 0 %和 5 2 0 0 %± 7 0 7%。给予TTX预处理后再加PD ,[Ca2 +]i也下降为起始值的 72 67%± 12 70 %。与单纯PD作用相比都有显著差异。结论 :PD可通过增加心肌 [Ca2 +]i而增强心肌收缩性 ,其作用可能与钙、钠通道开放有关。
AIM: To elucidate the mechanism of polydatin(PD) in increasing the contractility of myocardial cells by observing the cytosolic free calcium concentration ([Ca 2+ ]i) of myocardial cells of rats. METHODS: The cells were labelled with fluo-3-AM, and [Ca 2+ ]i was determined by use of confocal microscopy (ACAS 570). RESULTS: In the study, we found that [Ca 2+ ]i of myocytes was elevated 10min after adding PD (0.6 mmol/L), but [Ca 2+ ]i of some cells increased to 111.80%±2.22% vs baseline, the others to 224.00%±24.33%. The effect of PD was inhibited remarkably by pretreated with EGTA(2mmol/L), verapamil (50 μmol/L), a kind of L-calcium channel antagnist, and tetrodotoxin ( 1 μmol/L), a kind of sodium channel blocker 10 min before PD, the fluorescence value were decreased to 53.00%±9.02% , 52.00%±7.07% and 72.67%±12.70% respectively vs baseline (P<0 01). CONCLUSION: The results suggested that PD could increase [Ca 2+ ]i so as to enhance the contractility of myocardium, which might be related with the open of L-calcium channel and/or sodium channel.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2001年第2期128-130,共3页
Chinese Journal of Pathophysiology
基金
国家自然科学基金项目 (No .3 9870 93 6)
广东省博士启动基金资助 (No .984 0 97)
关键词
大鼠
心肌
钙
Rats
Myocardium
Calcium
