普萘洛尔对HUVEC-12细胞VGEF/ERK胞内信号转导影响  

Popranolol inhibits the VEGF inducing ERK expression in human umbilical vein endothelial cells

作　　者：鲁建云[1] 李锁[1] 黄进华[1] 康健[1] 向亚平[1] 秦桂芝[1] 陈静[1] 左成忻[1] 杨盛波[1] 谭丽娜[1] 赵婧[1] 

机构地区：[1]中南大学湘雅三医院皮肤科,湖南长沙410013

出　　处：《临床皮肤科杂志》2012年第10期587-589,共3页Journal of Clinical Dermatology

基　　金：湖南省自然科学基金(12JJ6086);长沙市科技局民生科技支撑专项基金(K1101026-31)

摘　　要：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 effects of propranolol on signaling transduction of VEGF/ERK in HUVEC-12 cell. Methods： The human umbilical vein endothelial cells （HUVEC-12） were used as culture model The different concentrations of propranolol were added to the culture medium. Then p-ERK1/2 expressions were assessed by Western blot. Results： The VEGF （at concentration of 20 μg/L） significant stimulated the p-ERK1/2 expressions in HUVEC-12 cell. The propranolol alone did not show any effect on the p-ERK1/2 expressions comparing with negative control. But, when HUVEC-12 cell were co-cultured with VEGF （20 μg/L）, the p-ERK1/2 expressions were significant inhibited in the propranolol treated cells at the concentrations of 8-16mg/L These concentrations of propranolol had no cytotoxic effect to cultured HUVEC-12 cell. Conclusion： The propranolol inhibits the p- ERK1/2 expressions induced by VEGF, which may be the mechanism of it inhibiting infantile haemangiomas in the clinic.

关 键 词：普萘洛尔 血管瘤 人血管内皮生长因子 细胞毒 ERK信号通路 

分 类 号：R394[医药卫生—医学遗传学]