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目的 探讨二氢吡啶类钙拮抗剂 2 ,6 二甲基 4 (3 硝基苯基 ) 1,4 二氢 3,5 吡啶二羧酸 3 甲酯 5 正戊酯(MN92 0 2 )增强红细胞 (RBC)变形性的可能机制。方法 角叉菜胶复制大鼠血栓模型 ;荧光染料Fura 2负载 ,荧光分光度法测定RBC内游离Ca2 +浓度 ;紫外分光光度法测定脂质过氧化产物丙二醛 (MDA)以及膜蛋白交联形成的共轭双烯的含量 ;孔雀绿法测定Ca MgATPase活力。 结果 MN92 0 2在本实验剂量范围内 ,剂量依赖地降低RBCMDA含量 (r =0 998) ,抑制膜共轭双烯的形成。MN92 0 2 0 1、1μmol·kg-1能增强全血SOD活力 ;有效抑制角叉菜胶引起的RBC内Ca2 +浓度的升高 ,但对RBCCa MgATPase活性无影响。结论 MN92 0 2阻断Ca2 +内流、抑制脂质过氧化是其改善RBC变形性的主要机制。
AIM: To investigate the effects of dihydropyridine calcium antagonist 2,6-dimethyl-4 (3-nitrophenyl) 1,4-dihydropyridine-3,5 dicarboxylate 5-n-pentyl ester (MN92 0 2) RBC) possible mechanism of deformability. Methods Carrageenan rat model of thrombosis was replicated. The free Ca 2+ concentration in RBC was measured by fluorescence spectrophotometry with Fura 2 and fluorescence spectrophotometry. The lipid peroxidation product malondialdehyde (MDA) and membrane protein were detected by ultraviolet spectrophotometry The formation of conjugated diene content; malachite green assay Ca MgATPase activity. Results MN92 0 2 reduced the RBCMDA content (r = 0 998) in a dose-dependent manner and inhibited the formation of membrane conjugated diolefins over the experimental dose range. MN92 0 2 0 1,1 μmol · kg-1 increased the activity of SOD in whole blood, inhibited the Ca2 + concentration in RBC induced by carrageenan effectively, but had no effect on the activity of RBCCa MgATPase. Conclusion MN92 0 2 block Ca2 + influx and inhibit lipid peroxidation is the main mechanism of improving the deformability of RBC.