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目的探讨17β雌二醇(E2)对去甲肾上腺素(NE)诱导的培养心肌细胞凋亡的影响及其可能机制。方法培养的新生大鼠心肌细胞分别给予NE(50μmol/L)、E2(10 nmol/L)、NE(50μmol/L)+E2(10 nmol/L)作用48 h,倒置相差显微镜和透射电镜观察心肌细胞形态结构的变化;DNA ladder和流式细胞术对心肌细胞凋亡情况进行定性和定量分析;免疫荧光细胞化学技术及半定量分析心肌细胞促凋亡基因c-fos的蛋白表达。结果E2抑制NE诱导的心肌细胞凋亡的特征性形态学改变如细胞萎缩,核染色质浓缩边集,线粒体肿胀,出现凋亡小体等;使凋亡心肌细胞特异性的DNA梯状条带消失;降低心肌细胞凋亡率并减弱凋亡心肌细胞内c-fos蛋白的表达。结论17β雌二醇可抑制去甲肾上腺素所诱导的心肌细胞凋亡,其机制可能与促凋亡基因c-fos的表达有关。
Objective To investigate the effect of 17β-estradiol (E2) on norepinephrine (NE) -induced cardiomyocyte apoptosis and its possible mechanism. Methods The cultured neonatal rat cardiomyocytes were treated with NE (50 μmol / L), E2 (10 nmol / L), NE (50 μmol / L) Cardiomyocytes morphological changes; DNA ladder and flow cytometry cardiomyocyte apoptosis qualitative and quantitative analysis; immunofluorescence cytochemistry and semi-quantitative analysis of myocardial cell apoptosis gene c-fos protein expression. Results E2 could inhibit the morphological changes of cardiomyocyte apoptosis induced by NE such as cell atrophy, chromatin condensation edge set, swelling of mitochondria, appearance of apoptotic bodies and so on. The specific DNA ladder of apoptotic cardiomyocytes Disappeared; decreased cardiomyocyte apoptosis rate and attenuated the expression of c-fos protein in apoptotic cardiomyocytes. Conclusion 17β-estradiol can inhibit noradrenaline-induced cardiomyocyte apoptosis, which may be related to the expression of pro-apoptotic gene c-fos.