前列腺素E_1对缺氧复氧乳鼠心肌细胞凋亡及bcl-2、bax蛋白表达的影响

目的:探讨前列腺素E1(PGE1)抑制缺氧复氧乳鼠心肌细胞凋亡的作用机制。方法:采用离体纯化培养的乳鼠心肌细胞建立缺氧复氧损伤模型,PGE1高、中、低各剂量组在缺氧复氧期分别给药;各组采用电镜技术和原位末端标记技术检测心肌细胞的凋亡情况,免疫组化技术检测bcl-2、bax蛋白表达情况。结果:与模型组比较,PGE1组心肌细胞的凋亡率显著降低,bcl-2蛋白表达明显上调而bax蛋白表达明显下调(P<0.01)。结论:离体培养的乳鼠心肌细胞建立的缺氧复氧损伤模型可诱导心肌细胞的凋亡,而PGE1可明显抑制这种凋亡的发生,其机制可能与促进bcl-2蛋白表达、抑制bax蛋白表达有关。

Effects of Prostaglandin E1 on Hypoxia/Reoxygenation Apoptosis and the Expression of bcl-2 and bax in Cardiocytes of the Neonate Rats

OBJECTIVE:To study the action mechanism of prostaglandin E1(PGE1)in the inhibition of hypoxia/reoxygenation apoptosis of cardiomyocytes in the cultured neonatal rats.METHODS:The hypoxia/reoxygenation model was made with the neonatal rat cardiomyocytes cultured by ex vivo purification,with drugs administered in PGE1(high,medium and low dosages)groups during hypoxia/reoxygenation.Hypoxia/reoxygenation apoptosis was studied by electron microscope and in situ end-labeling(ISEL).The expressions of bcl-2 and bax were detected by immunochemistry technique.RESULTS:In PGE1(high,medium and low dosages)groups compared with model group,the rate of apoptosis of cardiomyocytes decreased significantly,the expression of bac-2 increased significantly while the expression of bax decreased significantly(P<0.01).CONCLUSION:Hypoxia/reoxygenation injury model established by ex vivo purification culture of cardiomyocytes of neonatal rats can induce cardiomyocyte apoptosis,while PGE1 can significantly inhibit the cardiomyocyte apoptosis,the mechanisms are possibly due to the increasing of the expression of bcl-2 and inhibition of the expression of bax.