CAJ | 학술논문

目的：研究SKF96365和氯化镍（NiCl2）对环匹阿尼酸（CPA）诱导的大鼠远端肺动脉平滑肌细胞（PASMC）内游离钙离子浓度（[Ca2＋]i）变化的影响。方法培养大鼠PASMC，运用荧光显微镜和InCyte细胞内钙浓度检测系统观测CPA、SKF96365和NiCl2对PASMC[Ca2＋]i的影响。结果含5μmol／L硝苯地平的无钙Krebs溶液孵育PASMC，10μmol／LCPA使PASMC[Ca2＋]i短暂小幅升高，恢复细胞外Ca2＋至2．5mmol／L后，10μmol／LCPA使PASMC[Ca2＋]i迅速显著升高；50μmol／LSKF96365和500μmol／LNiCl2均能明显抑制10μmol／LCPA引起的PASMC[Ca2＋]i升高，但对高钾（60mmol／LKCl）溶液引起的PASMC[Ca2＋]i升高无影响。结论CPA可致大鼠PASMC[Ca2＋]i升高，且能被SKF96365和NiCl2阻断，提示CPA可能诱发细胞外Ca2＋经钙池操纵性钙通道（SOCC）内流，SKF96365和NiCl2能选择性抑制SOCC活性使经SOCC的Ca2＋内流减少。
목적：연구SKF96365화록화얼（NiCl2）대배필아니산（CPA）유도적대서원단폐동맥평활기세포（PASMC）내유리개리자농도（[Ca2＋]i）변화적영향。방법배양대서PASMC，운용형광현미경화InCyte세포내개농도검측계통관측CPA、SKF96365화NiCl2대PASMC[Ca2＋]i적영향。결과함5μmol／L초분지평적무개Krebs용액부육PASMC，10μmol／LCPA사PASMC[Ca2＋]i단잠소폭승고，회복세포외Ca2＋지2．5mmol／L후，10μmol／LCPA사PASMC[Ca2＋]i신속현저승고；50μmol／LSKF96365화500μmol／LNiCl2균능명현억제10μmol／LCPA인기적PASMC[Ca2＋]i승고，단대고갑（60mmol／LKCl）용액인기적PASMC[Ca2＋]i승고무영향。결론CPA가치대서PASMC[Ca2＋]i승고，차능피SKF96365화NiCl2조단，제시CPA가능유발세포외Ca2＋경개지조종성개통도（SOCC）내류，SKF96365화NiCl2능선택성억제SOCC활성사경SOCC적Ca2＋내류감소。
Objective To study the effect of SKF96365 and NiCl2 on cyclopiazonic acid (CPA) induced intracellular calcium cation concentration ([Ca2+ ]i ) change in rat distal pulmonary arterial smooth muscle cells (PASMC) .Methods The rat distal PASMC were isolated and cultured .The effects of CPA ,SKF96365 and NiCl2 on [Ca2+ ]i in PASMC were tested by fluorescence microscope and InCyte [Ca2+ ]i measurement system .Results PASMC were incubated with Ca2+‐free Krebs solution containing 5μmol/L nifedipine ,10 μmol/L CPA caused a small transient increase in [Ca2+ ]i ;after restoration of extracellular Ca2+ to 2 .5 mmol/L ,10 μmol/L CPA caused marked increases in [Ca2+ ]i in PASMC incubated with Krebs solution containing 5 μmol/L nife‐dipine .Both 50 μmol/L SKF96365 and 500 μmol/L NiCl2 distinctly attenuated the increases in [Ca2+ ]i caused by 10 μmol/L CPA in PASMC .However ,neither 50 μmol/L SKF96365 nor 500 μmol/L NiCl2 affected the increases in [Ca2+ ]i caused by 60 mmol/L KCl in PASMC .Conclusion CPA induced increases in [Ca2+ ]i may related to Ca2+ release from sarcoplasmic reticulum and the in‐flux of Ca2+ through store‐operated Ca2+ channels (SOCC) in rat distal PASMC .Both SKF96365 and NiCl2 could selectively block SOCC and attenuated the influx of Ca2+ through SOCC in PASMC .