摘要
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。
The effects of low density lipoprotein (LDL) on intracellular calcium concentration ([Ca^(2+)] i) of fat-storing cells (FSCs) in rats and the interference of calcium antagonists induced by LDL were studied. Flnrescent spectrophotometry and Fura-2/AM were used to determine the dose-response of LDL on peak [ Ca^(2+)] i in FSCs and the effects of LDL on [ Ca^(2+) ] i in conditions with or without Ca^(2+) in the extracellular. At the same time, we observed the effects of calcium antagonists on LDL induced calcium response. Results showed LDL could induce [ Ca^(2+)] i dose-dependent increase in FSCs. The [Ca^(2+)] i level reached a maximal value when the LDL concentration was 100 μg/ml. LDL could apparently and quickly increase the [Ca^(2+)] i in conditions with or without extracellular Ca^(2+). Also nicardipine and verapamil had the effects of down-regulation of the Ca^(2+)-response induced by LDL in FSCs. Conclusion: LDL could induce an elevation of the [ Ca^(2+)] i in FSCs. LDL could modulate the proliferation and extracellular matrix production of FSCs by calcium channel.
出处
《上海第二医科大学学报》
CSCD
1998年第1期41-43,共3页
Acta Universitatis Medicinalis Secondae Shanghai
关键词
贮脂细胞
低密度脂蛋白
钙离子
fat-storing cell
low density lipoprotein
calciumion
