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研究低密度脂蛋白(LDL)对大鼠肝脏贮脂细胞(FSC)胞内钙离子(Ca~(2+))浓度的影响及钙拮抗剂对其的干预作用。采用Fura-2/AM标记法检测不同浓度LDL(10、25、50、100、200、500μg/ml)对FSC胞内Ca~(2+)浓度峰值的影响及在细胞外液含钙或不含钙时.100μg/ml LDL剂量组对FSC胞内Ca~(2+)浓度的影响,同时测定钙拮抗剂尼卡地平(Nic)和维拉帕米(Ver)对LDL引起增钙的拮抗作用。结果:LDL能刺激FSC胞内Ca~(2+)浓度达最高值,在细胞外液含钙或不含钙时.LDL均可在很短时间内明显升高胞内Ca~(2+)浓度。Nic和Ver能明显抑制LDL引起的增钙作用。结论:LDL能刺激FSC胞内Ca~(2+)浓度升高,其可能通过钙通道对FSC增殖、合成细胞外基质进行调控。
To study the effects of low density lipoprotein (LDL) on intracellular calcium (Ca2 +) concentration in rat liver fat-storing cells (FSC) and the effect of calcium antagonist on it. Fura-2 / AM labeling method was used to detect the effect of different concentration of LDL (10,25,50,100,200,500μg / ml) on the intracellular concentration of Ca 2+ in FSC and the effect of calcium concentration in the extracellular solution Calcium, 100μg / ml LDL dose group on the concentration of intracellular Ca 2+ in FSC, and at the same time, the antagonism of Nicardipine (Nic) and verapamil (Ver) effect. Results: LDL stimulated the intracellular Ca 2+ concentration in FSC to the highest level, while in the extracellular Ca 2+ or in the absence of calcium, LDL significantly increased intracellular Ca 2+ concentration in a short time, concentration. Nic and Ver significantly inhibited the calcium-adding effect caused by LDL. Conclusion: LDL can stimulate the increase of Ca 2+ concentration in FSC, which may regulate the proliferation of FSC and the synthesis of extracellular matrix through calcium channel.