丙泊酚通过MAPK/ERK途径抑制食管癌细胞系EC9706中VEGF的表达
投稿时间:2017-04-10  修订日期:2017-04-12  点此下载全文
引用本文:杨国庆,刘德军.丙泊酚通过MAPK/ERK途径抑制食管癌细胞系EC9706中VEGF的表达[J].医学研究杂志,2017,46(12):90-94
DOI: 10.11969/j.issn.1673-548X.2017.12.023
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作者单位E-mail
杨国庆 712000 西安, 陕西中医药大学第二附属医院麻醉科  
刘德军 712000 西安, 陕西中医药大学第二附属医院心脏外科 yangguoqing19808@163.com 
基金项目:陕西省咸阳市卫生局科技计划项目(J2015163)
中文摘要:目的 探究丙泊酚对食管癌细胞系EC9706中血管内皮生长因子VEGF表达情况的影响及相关分子机制。方法 通过蛋白免疫印迹检测人食管癌细胞系EC9706与正常食管上皮细胞系HEEC中VEGF表达情况。分别用不同浓度的丙泊酚(0、2、6、10μg/L)培养EC9706,孵育后,对各组EC9706细胞株行MTT、流式细胞术、细胞侵袭实验、细胞划痕修复试验,观察各组细胞增殖、凋亡、侵袭和迁移能力;使用qRT-PCR和蛋白免疫印迹分别检测各组细胞内VEGF、p38(MAPK)和p44/42(ERK1/2)的表达和磷酸化水平。结果 EC9706细胞中VEGF表达显著强于HEEC细胞。丙泊酚干预后,丙泊酚组细胞增殖、迁移和侵袭显著低于Ctrl组;而丙泊酚组细胞凋亡率显著高于Ctrl组。qRT-PCR和蛋白免疫印迹结果显示,丙泊酚组瘤细胞内VEGF mRNA和蛋白表达水平显著降低;丙泊酚抑制p38(MAPK)和p44/42(ERK1/2)的表达和磷酸化水平。上述这些影响都存在剂量依赖性。结论 丙泊酚抑制人食管癌细胞系EC9706的增殖、侵袭和迁移,促进细胞凋亡。其潜在的机制是通过抑制MAPK/ERK信号通路,进而抑制VEGF的表达。
中文关键词:丙泊酚  食管癌细胞系EC9706  MAPK/ERK途径  VEGF
 
Propofol Inhibiting the Expression of VEGF through MAPK/ERK Signal Pathways in Oesophageal Carcinoma Cells EC9706
Abstract:Objective To investigate the effect of propofol on the expression of VEGF in Oesophageal carcinoma cells EC9706 and its related molecular mechanism.Methods The expression of VEGF in human Oesophageal carcinoma cells EC9706 and normal esophageal epithelium cells HEEC were compared by immunoblotting. EC9706 was treated with different concentrations of propofol (0,2,6,10μg/L). After incubation, the EC9706 cell lines were detected with MTT, flow cytometry, cell invasion and cell scratch tests. The expression of VEGF, and the phosphorylation of p38 (MAPK) and p44/42 (ERK1/2) were detected by qRT-PCR and immunoblotting in each group.Results The expression of VEGF in EC9706 cells was significantly higher than that in HEEC cells. After propofol intervention, the proliferation, migration and invasion of propofol groups were significantly lower than that of Ctrl group, while the apoptotic rate of propofol groups were significantly higher than that of Ctrl group. The expression of VEGF mRNA and protein in propofol groups were significantly lower than that in Ctrl group. The expression and phosphorylation of p38 (MAPK) and p44/42 (ERK1/2) were inhibited by propofol. Both of these effects were dose-dependent.Conclusion Propofol inhibits the proliferation, invasion and migration of OC cells EC9706 and promotes apoptosis. Its potential mechanism may work by inhibiting the MAPK/ERK signaling pathway, thereby inhibiting VEGF expression.
keywords:Propofol  Oesophageal carcinoma cells EC9706  MAPK/ERK pathway  VEGF
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