【摘要】 目的:探讨大鼠结肠平滑肌细胞是否存在钙库操纵性通道(SOC)。方法:荧光探针Fura-2/AM标记细胞内游离Ca2+后,用荧光分光光度计检测毒胡萝卜素(thapsigargin)和咖啡因(caffeine)耗竭胞内钙库后激活的SOC通道对酶解分离的大鼠结肠平滑肌细胞[Ca2+]i的影响。结果:在无Ca2+缓冲液中,thapsigargin(1μmol/L)以及caf-feine(10 mmol/L)分别使[Ca2+]i由静息时(68.32±3.43)nmol/L升高至(240.85±12.65)nmol/L(、481.25±34.77)nmol/L,继之,向细胞外液中引入两种浓度的Ca2+(1.5 mmol/L和3.0 mmol/L),导致[Ca2+]i进一步升高,分别为(457.55±19.80)nmol/L、(1005.93±54.62)nmol/L;(643.88±34.65)nmol/L、(920.16±43.25)nmol/L。且上述升高效应对维拉帕米(verapamil,5μmol/L)以及KCl引起的细胞膜去极化不敏感,但可被La3+(1 mmol/L)抑制。结论:在酶解分离的大鼠结肠平滑肌细胞上,存在胞内钙库耗竭激活的SOC通道,为支持在电兴奋性细胞上存在库容性Ca2+内流提供了实验和理论依据。更多还原

【Abstract】 Aim: To study whether store-operated Ca²⁺ channel（SOC） is present in rat colonic smooth muscle cells.Methods: Intracellualr Ca²⁺([Ca²⁺]i) changes induced by thapsigargin-or caffeine-activated SOC channel were measured in enyzmatically dissocia（ted） rat colonic smooth muscle cells with the fluorescent indicator Fura-2/AM.Results: In the absence of external Ca²⁺,the sarco-endoplasmic reticulum Ca²⁺ pump inhibitor thapsigargin（1 μmol/L） and ryanodine receptor（RyR） activator caffeine both transiently elevated [Ca²⁺]i from（68.32 ±3.43） nmol/L to（240.85±12.65 ）nmol/L,（481.25±34.77） nmol/L.A subsequent reintroduction of Ca²⁺ into the extracellular solution resulted in [Ca²⁺]i furthur elevated to（457.55±19.80） nmol/L、（1005.93±54.62） nmol/L;（643.88±34.65） nmol/L、（920.16±43.25） nmol/L,respectively.And the elevated response was blocked by lanthanum（1 mmol/L）,but was insensitive to L-type voltage calcium channels blocker verapamil and membrane depolarization.Conclusion: SOC activated by store depletion are present in rat colonic smooth muscle cells.And we further prove the existence of such Ca²⁺ channels in excitable cells.更多还原