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目的:通过血管内皮生长因子/细胞外信号调节激酶(VEGF/ERK)的胞内信号转导途径研究普萘洛尔治疗血管瘤的疗效机制。方法:以离体培养的人脐静脉内皮细胞(HUVEC-12)为模型,观察普萘洛尔对体外培养内皮细胞磷酸化ERK影响。摸索合适的重组人VEGF浓度,建立HUVEC-12细胞VEGF阳性系统,在其基础上采用四甲基偶氮唑蓝法测定普萘洛尔对VEGF阳性系统HUVEC-12细胞的细胞毒作用及蛋白质免疫印迹法测ERK变化。结果:普萘洛尔对体外培养内皮细胞磷酸化ERK影响差异无统计学意义。VEGF在20μg/L时HUVEC-12细胞磷酸化ERK表达最强,以该浓度建立HUVEC-12细胞VEGF阳性系统。与空白对照组相比,普萘洛尔对VEGF阳性系统的HUVEC-12细胞细胞毒作用差异无统计学意义(P>0.05);在普萘洛尔浓度为8～16 mg/L时磷酸化ERK表达受到抑制。结论:普萘洛尔治疗血管瘤的机制可能为通过抑制VEGF诱导的内皮细胞的胞内ERK信号转导,从而促进血管瘤的消退。
OBJECTIVE: To investigate the therapeutic mechanism of propranolol in the treatment of hemangiomas by the intracellular signal transduction pathway of vascular endothelial growth factor / extracellular signal-regulated kinase (VEGF / ERK). Methods: Human umbilical vein endothelial cells (HUVEC-12) cultured in vitro were used as models to observe the effects of propranolol on ERK phosphorylation in cultured endothelial cells. Appropriate recombinant human VEGF concentration was explored to establish a VEGF-positive system of HUVEC-12 cells. Based on this, the cytotoxicity and protein immunization of propranolol on VEGF-positive HUVEC-12 cells were determined by MTT assay Imprinting method to measure ERK changes. RESULTS: Propranolol had no significant effect on phosphorylated ERK in cultured endothelial cells in vitro. The phosphorylation of ERK was the strongest in HUVEC-12 cells with 20μg / L VEGF, and the VEGF positive system of HUVEC-12 cells was established at this concentration. Compared with the blank control group, there was no significant difference in the cytotoxic effect of propranolol on VEGF-positive HUVEC-12 cells (P> 0.05). When propranolol was 8-16 mg / L, phosphorylation ERK expression was inhibited. CONCLUSIONS: The mechanism of propranolol in the treatment of hemangiomas may be to promote the regression of hemangiomas by inhibiting VEGF-induced intracellular ERK signaling in endothelial cells.