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目的:探讨缺血缺氧状态下细胞外信号调节激酶(Extranal-signal regulated kinase1/2,ERK1/2)的活化及其对心肌细胞分泌偶联因子-6(CF6)的影响。方法:培养的乳鼠心肌细胞随机分为3组:正常对照组(正常培养的心肌细胞);缺血缺氧组;U0126组:缺血缺氧加U0126(ERK1/2特异性抑制剂)。于刺激后6h收集标本进行检测。采用放射免疫法检测培养基中CF6的含量;使用Western Blots方法检测心肌细胞磷酸化ERK1/2激酶的蛋白含量。结果:缺血缺氧刺激6h后,心肌细胞培养液上清中CF6的含量比正常对照组明显增加(P<0.01);ERK1/2抑制剂能够抑制缺血缺氧诱导的ERK1/2磷酸化;同时,缺血缺氧诱导的CF6分泌增加可被ERK1/2抑制,其抑制率为40.2%(P<0.01)。结论:缺血缺氧刺激可上调体外培养的大鼠心肌细胞CF6的分泌;ERK1/2激酶的活化与心肌细胞CF6释放调节有关。
Objective: To investigate the activation of extracellular signal-regulated kinase (ERK1 / 2) and its effect on cardiomyocyte secretion of coupling factor-6 (CF6) during hypoxia-ischemia. Methods: The cultured neonatal rat cardiomyocytes were randomly divided into 3 groups: normal control group (normal cultured cardiomyocytes); ischemia / hypoxia group; U0126 group: hypoxia / hypoxia plus U0126 (ERK1 / 2 specific inhibitor). 6h after stimulation to collect specimens for testing. The content of CF6 in culture medium was detected by radioimmunoassay. The protein content of phosphorylated ERK1 / 2 kinase in myocardial cells was detected by Western Blots. Results: The content of CF6 in the culture supernatant of cardiomyocytes increased significantly (P <0.01) 6 h after hypoxia / hypoxia stimulation. ERK1 / 2 inhibitor could inhibit the phosphorylation of ERK1 / 2 induced by hypoxia and hypoxia At the same time, the increase of CF6 secretion induced by hypoxia and hypoxia could be inhibited by ERK1 / 2 with the inhibition rate of 40.2% (P <0.01). CONCLUSION: Ischemia and hypoxia can up-regulate the secretion of CF6 in rat cardiomyocytes cultured in vitro. The activation of ERK1 / 2 kinase is related to the regulation of CF6 release from cardiomyocytes.