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作 者:金春华[1] 赵克森[1] 刘杰[1] 黄辉[1] 朱佐江[1] 黄绪亮[1]
机构地区:[1]第一军医大学病理生理教研室
出 处:《中国病理生理杂志》1998年第2期195-198,共4页Chinese Journal of Pathophysiology
摘 要:目的:观察虎杖甙(PD)对培养的大鼠血管平滑肌细胞(VSMC)内钙离子浓度的变化机理。方法:用Fluo-3-AM标记培养的VSMC,在粘附式细胞仪上测定细胞内游离钙的变化。结果:实验结果表明,PD(002~20mmol/L)可使大鼠VSMC内游离钙浓度升高,波形变宽,其引起的钙波形态与去甲肾上腺素(NE)及氯化钾所引起的高尖钙波不同,PD使VSMC产生一种剂量依赖性的、持续缓慢升高的钙波。PD引起的细胞内游离钙升高可被EGTA(2mmol/L)及维拉帕米(50μmol/L)明显抑制。结论:以上结果提示PD既促进VSMC外钙离子进入细胞内,还能诱导细胞内钙离子释放;PD可能会提高正常VSMC的收缩性,增加正常血管的张力。AIM:The present study was to investigate the mechanism of polydatin effects on vessels. METHODS:The changes of the cytosolic free calcium concentration of cultured vascular smooth muscle cells (VSMC)were determined kinetically from rat aorta.RESULTS:It was found that polydatin caused a persistent and dose-dependent increase of intracellular calcium concentration[Ca 2+ ]i,which were inhibited partly by pretreatment with calcium chelator EGTA(2 mmol/L) and calcium channel blocker verapamil(50 μmol/L)respectively 10 min prior to polydatin administration. CONCLUSION:The results suggested that polydatin-induced [Ca 2+ ]i alternation are not only due to extracellular Ca 2+ inflow but also Ca 2+ release from intracellular calcium store.
分 类 号:R543[医药卫生—心血管疾病] R285.5[医药卫生—内科学]
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