文章摘要
臧 婷,王晓毅,李紫薇,王小雨,彭余楠.七氟烷预处理对肺癌细胞凋亡与增殖的影响及机制分析[J].,2020,(8):1416-1419
七氟烷预处理对肺癌细胞凋亡与增殖的影响及机制分析
Effects of Sevoflurane Preconditioning on Apoptosis and Proliferation of Lung Cancer Cells and Its Mechanism
投稿时间:2019-12-01  修订日期:2019-12-26
DOI:10.13241/j.cnki.pmb.2020.08.004
中文关键词: 七氟烷  肺癌  细胞凋亡  细胞增殖  SDF-1/CXCR7信号通路
英文关键词: Sevoflurane  Lung cancer  apoptosis  Cell proliferation  SDF-1/CXCR7signal pathway
基金项目:江苏省自然科学基金项目(2017J0356)
作者单位E-mail
臧 婷 南京大学医学院附属南京鼓楼医院麻醉科 江苏 南京 210008 ztt19870323@163.com 
王晓毅 南京大学医学院附属南京鼓楼医院麻醉科 江苏 南京 210008  
李紫薇 徐州医学院附属医院麻醉科 江苏 徐州 221000  
王小雨 南京大学医学院附属南京鼓楼医院麻醉科 江苏 南京 210008  
彭余楠 南京大学医学院附属南京鼓楼医院麻醉科 江苏 南京 210008  
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中文摘要:
      摘要 目的:探讨与分析七氟烷预处理对肺癌细胞凋亡与增殖的影响及机制。方法:采用不同浓度的七氟烷处理肺癌细胞系A549,采用噻唑蓝法检测细胞增殖抑制情况,流式细胞术检测细胞凋亡,Transwell实验检测细胞转移与侵袭,采用免疫印迹法明确七氟烷的具体作用机制。结果:七氟烷处理可导致A549细胞增殖率显著降低,细胞凋亡率显著增加(P<0.05),且存在剂量依赖性(P<0.05)。同时细胞转移与侵袭指数、基质细胞衍生因子-1(Stromal cell-derived factor 1,SDF-1)、CXC类趋化因子受体7(CXC chemokine receptor 7,CXCR7)蛋白相对表达量显著降低(P<0.05),也存在剂量依赖性(P<0.05)。结论:七氟烷预处理能抑制肺癌细胞的SDF-1/CXCR7信号通路,从而促进细胞凋亡,抑制细胞增殖、转移与侵袭。
英文摘要:
      ABSTRACT Objective: To investigate and analysis the effects of sevoflurane preconditioning on apoptosis and proliferation of lung cancer cells. Methods: The lung cancer cell line A549 were treated with different concentrations of sevoflurane. The inhibition of cell proliferation were detected by thiazolyl blue method. The apoptosis were detected by flow cytometry. The cell transfer and invasion were detected by Transwell assay. The sevoflurane were identified by immunoblotting. Results: The treatment of sevoflurane resulted in significant decreased in the proliferation rate of A549 cells (P<0.05), and were significant increased in apoptosis rate (P<0.05), and there were dose-dependent (P<0.05). At the same time, the relative expression of cell transfer and invasion index, Stromal cell-derived factor 1(SDF-1) and CXC chemokine receptor 7(CXCR7) protein were significantly decreased (P<0.05), and there were also dose-dependent (P<0.05). Conclusion: Sevoflurane preconditioning can inhibit the SDF-1/CXCR7 signaling pathway in lung cancer cells, thereby promoting apoptosis and inhibiting cell proliferation, metastasis and invasion.
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