Article Summary
秦萌萌,高 莹,李昕玲,宋 迪,王琳琳.白藜芦醇通过下调MEK/ERK/c-Jun信号通路抑制H2O2诱导的肺癌细胞增殖[J].现代生物医学进展英文版,2020,(3):465-469.
白藜芦醇通过下调MEK/ERK/c-Jun信号通路抑制H2O2诱导的肺癌细胞增殖
Resveratrol Inhibits H2O2-induced Proliferation of Lung Cancer Cells by Down-regulating MEK/ERK/c-Jun Signal Pathway
Received:April 24, 2019  Revised:May 18, 2019
DOI:10.13241/j.cnki.pmb.2020.03.013
中文关键词: 白藜芦醇  过氧化氢  肺癌  细胞增殖  MEK/ERK/c-Jun  信号通路
英文关键词: Resveratrol  H2O2  Lung cancer  Cell proliferation  MEK/ERK/c-Jun  Signaling pathway
基金项目:辽宁省自然科学基金指导计划项目(201602812)
Author NameAffiliationE-mail
QIN Meng-meng Department of Respiratory and Critical Care Medicine, General Hospital of Northern Theater Command of PLA, Shenyang, Liaoning, 110016, China meng2012vip@sohu.com 
GAO Ying Department of Respiratory and Critical Care Medicine, General Hospital of Northern Theater Command of PLA, Shenyang, Liaoning, 110016, China  
LI Xin-ling Department of Respiratory and Critical Care Medicine, General Hospital of Northern Theater Command of PLA, Shenyang, Liaoning, 110016, China  
SONG Di Department of Respiratory and Critical Care Medicine, General Hospital of Northern Theater Command of PLA, Shenyang, Liaoning, 110016, China  
WANG Lin-lin Department of Respiratory and Critical Care Medicine, General Hospital of Northern Theater Command of PLA, Shenyang, Liaoning, 110016, China  
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中文摘要:
      摘要 目的:探讨白藜芦醇(Res)是否通过下调ERK激酶/胞外信号调节激酶/原癌基因(MEK/ERK/c-Jun)信号通路抑制小剂量过氧化氢(H2O2)诱导肺癌细胞增殖。方法:采用MTS实验检测小剂量20 μM H2O2以及分别加入MEK阻断剂U0126和Res后H2O2对肺癌细胞NCI-H1395增殖的影响,采用Western Blot检测H2O2对ERK1/2和Akt蛋白磷酸化水平以及加入Res后H2O2对MEK、ERK1/2和c-Jun蛋白磷酸化水平的影响。结果:小剂量H2O2对肺癌细胞NCI-H1395具有促增殖作用,H2O2通过活化ERK1/2和Akt蛋白的磷酸化水平促进肺癌细胞NCI-H1395增殖,加入MEK阻断剂U0126后H2O2对肺癌细胞NCI-H1395增殖作用降低(P<0.05)。Res可抑制H2O2诱导的肺癌细胞NCI-H1395增殖,加入Res后,H2O2引起的MEK、ERK1/2和c-Jun蛋白磷酸化水平均降低(P<0.05)。结论:小剂量H2O2对肺癌细胞NCI-H1395具有促增殖作用,Res通过抑制MEK/ERK/c-Jun信号通路来抑制H2O2对肺癌细胞NCI-H1395的促增殖作用,其具体机制还需进一步研究。
英文摘要:
      ABSTRACT Objective: To investigate whether resveratrol (Res) can inhibit low-dose hydrogen peroxide (H2O2) induced proliferation of lung cancer cells by down regulating the ERK kinase/extracellular signal regulated kinase/proto oncogene (MEK/ERK/c-Jun) signal pathway. Methods: The effect of H2O2 on the proliferation of lung cancer cell line NCI-H1395 with low-dose 20 μm H2O2 and after adding MEK blocking agent U0126 and Res were detected by MTS assay. The effect of H2O2 on the phosphorylation of ERK1/2 and Akt protein and the effect of H2O2 on the phosphorylation of MEK, ERK1/2 and c-Jun after adding Res were detected by Western Blot. Results:: Low-dose H2O2 could promote the proliferation of lung cancer cell line NCI-H1395, and H2O2 promoted the proliferation of lung cancer cell line NCI-H1395 by activating the phosphorylation of ERK1/2 and Akt protein. After adding MEK inhibitor U0126, the effect of H2O2 on the proliferation of lung cancer cell line NCI-H1395 was decreased (P<0.05). Res could inhibit H2O2 induced proliferation of lung cancer cell line NCI-H1395. After adding Res, the effects of H2O2 on the phosphorylation of MEK, ERK1/2 and c-Jun protein were decreased (P<0.05). Conclusion: Low-dose H2O2 can promote the proliferation of lung cancer cell line NCI-H1395, and Res can inhibit H2O2 induced the proliferation of lung cancer cell line NCI-H1395 by inhibiting MEK/ERK/c-Jun signaling pathway, but the specific mechanism still needs further study.
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