Urocortin调控Bcl-2家族与大鼠缺氧/复氧心肌细胞凋亡

目的观察神经肽Urocortin对大鼠缺氧/复氧心肌细胞Bcl-2及相关基因mRNA表达和细胞凋亡的影响。方法培养新生大鼠的心肌细胞并缺氧/复氧处理,用RT-PCR检测Bcl-2、Bax、Bcl-xL、Bad mRNA表达,TUNEL法检测细胞凋亡。结果Urocortin治疗组Bcl-2的mRNA表达与缺氧/复氧组比较明显增加(P<0.05),Bax的表达明显下降(P<0.05),Bcl-xL、Bad mRNA表达无明显改变(P>0.05)。Urocortin治疗组凋亡细胞率与缺氧/复氧组比较减少(P<0.05)。结论Urocortin调节心肌细胞Bcl-2家族基因转录下凋促凋亡基因Bax表达,上调抑凋亡基因Bcl-2使Bcl-2/Bax比值增加。这可能是Urocortin抗大鼠缺氧/复氧心肌细胞凋亡的机制之一。

The Effect of Urocortin on Bcl-2 Family Members Transcription and Apoptosis of Cardiomyocytes after Hypoxia and Reoxygenation

Objective: To investigate the effects of Urocortin on Bcl-2 family mRNA expression and apoptosis of cardiomyocytes after hypoxia and reoxygenation (H/R).Method: Isolated and cultured rat cardiomyocytes were divided to three groups : normal control,H/R and H/R Urocortin. In H/R Urocortin group, cardiomyocytes were pretreated with Urocortin for 30 min and then subjected to continuous hypoxic injury for 6 hours or 12 hours, followed by reoxygenation for 2 hours. Cardiomyocytes apoptosis was measured by TUNEL. Bcl-2,Bax, Bcl-xL and Bad mRNA expression is measured by RT-PCR.Results: Positive cell rate of TUNEL in H/R Urocortin was significantly lower than that of H/R group. The mRNA expression of Bcl-2 in H/R Urocortin was significantly higher than that of H/R group (P<0.05). Bax mRNA expression in H/R Urocortin was significantly lower than that of H/R group (P<0.05). Urocortin pretreatment did not change Bcl-xL and Bad mRNA levels in cardiomyocytes after hypoxia and reoxygenation (P>0.05).Conclusion: Urocortin can reduce culture rat cardiomyocytes apoptosis after hypoxia and reoxygenation. This effect may be associated with the regulation of Bcl-2 and Bax genes expression by Urocortin.