论文部分内容阅读
目的 :在培养的乳鼠心肌细胞缺氧 /复氧 (anoxia/reperfusion ,A/R)损伤模型上 ,观察金属硫蛋白(MT)在碱性成纤维细胞生长因子 (bFGF)心肌保护中的作用 ,探讨bFGF心肌保护作用的可能机制。方法 :用bFGF(10 -10 、10 -9、10 -8mol/L)及同时应用PD0 980 59的bFGF(10 -9mol/L)预孵育乳鼠心肌细胞 2 4h ,复制心肌细胞A/R损伤模型 ,光镜下计算细胞存活率 ,[10 9Cd]-血红素饱和法测细胞MT含量 ,硫代巴比妥酸法测细胞丙二醛(MDA)含量 ,以自动生化分析仪测培养液乳酸脱氢酶 (LDH)活性。结果 :bFGF呈浓度依赖地诱导心肌细胞MT生成 ,10 -10 、10 -9、10 -8MbFGF组MT含量分别高于A/R组 5 4%、6 2 %、76 % ,并拮抗A/R引起的细胞损伤 ,细胞存活率高于A/R组 ,细胞乳酸脱氢酶 (LDH)及蛋白漏出较少 ,细胞丙二醛 (MDA)含量低于A/R组 ,而用丝裂素活化蛋白激酶 (MAPK)抑制剂PD0 980 59抑制MT生成则减弱了bFGF的上述细胞保护作用。结论 :MT参与了bFGF的心肌保护作用 ,并与MAPK的介导有关。
OBJECTIVE: To observe the effect of metallothionein (MT) on myocardial protection of basic fibroblast growth factor (bFGF) in cultured neonatal rat cardiomyocytes subjected to anoxia / reperfusion (A / R) injury model , To explore the possible mechanism of myocardial protection of bFGF. Methods: The neonatal rat cardiomyocytes were preincubated with bFGF (10 -10, 10 -9, 10 -8 mol / L) and bFGF (10 -9 mol / L) The cell viability was calculated under light microscope. The content of MT was measured by [10 9Cd] -hemoglobin saturation method and the malondialdehyde (MDA) content was measured by thiobarbituric acid method. The content of lactate Dehydrogenase (LDH) activity. Results: The MTF of cardiomyocytes was induced by bFGF in a dose-dependent manner. MT contents in 10 -10, 10 -9 and 10 -8 MbFGF groups were 54%, 62% and 76% Induced cell injury and cell survival rate were higher than those in A / R group, the cell lactate dehydrogenase (LDH) and protein leakage were less, the content of malondialdehyde (MDA) in cells was lower than that in A / R group, Inhibition of MT production by the protein kinase (MAPK) inhibitor PD0 980 59 attenuated the above cytoprotective effects of bFGF. Conclusion: MT is involved in myocardial protection of bFGF and is involved in the mediation of MAPK.