摘要
本实验用激光扫描共聚焦技术发现肿瘤坏死因子（１ＭＩＵ·Ｌ－１）使培养的单个血管内皮细胞胞浆区和核区Ｃａ２＋皆呈现一过性升高，而且核区上升幅度大，下降缓慢。同等剂量的肿瘤坏死因子没有引起单个白细胞Ｃａ２＋水平的明显变化。蛋白激酶Ｃ的活化剂佛波醇酯（３．５ｎｍｏｌ·Ｌ－１）可引起两类细胞Ｃａ２＋水平皆迅速升高，随后下降，低于原水平，最后，内皮细胞核区Ｃａ２＋完全被排空，而白细胞核区仍残留Ｃａ２＋。结果提示肿瘤坏死因子对不同的靶细胞的刺激效应不同；细胞不同区的Ｃａ２＋水平变化效应也不同；蛋白激酶Ｃ的作用主要是排出细胞内Ｃａ２＋。观察单个细胞Ｃａ２＋变化有助于研究Ｃａ２＋参与动脉粥样硬化发病机制。
In present experiment the temporal increase of the calcium level both in cytoplasma and nuclear of single culture endothelial cell was observed after stimulation of tumor necrosis factor-a (TNFa, 1MIU·L-1), however, the increase of calcium level was more significant in nuclear and decreased slowly. The calcium level was not changed obviously in white cell after stimulation of TNFa in same dosage. The calcium level both in endothelial cell and white cell increased rapidly and ten decreased less than the original level alter stimulation of phorbol myristate acetate (3. 5nmol·L-1 ) which is a activator for protein kinase C (PKC). Finally, it was found that the nuclear calcium of endothelial cell was output entirely, but there was calcium reside in the n[lclear of white cell. The results suggested that the effects of TNFa stimulation are different on the different kinds of target cells. the changes of calcium level are different in different region of cell,and the PKC plays an important role in the calcium output from inside of the cell.but it may don't participate in the offect of TNFa on the cell calcium. Investigating the calcium change in the single endothelinalcell should benefit the research on the role of Ca2+ in the pathogenesis of atherosclerosis.
出处
《中国动脉硬化杂志》
CAS
CSCD
1995年第1期1-4,共4页
Chinese Journal of Arteriosclerosis
基金
国家自然科学基金
关键词
动脉粥样硬化
细胞钙
肿瘤坏死因子
蛋白激酶C
Cytosolic calcium: Tumor necrosis factor
Protein kinase C
Laser confocal scanning
