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

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20μM 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。

Resveratrol Inhibits H2O2-induced Proliferation of Lung Cancer Cells by Down-regulating MEK/ERK/c-Jun Signal Pathway

Objective: To investigate whether resveratrol(Res) can inhibit low-dose hydrogen peroxide(H2 O2) 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 H2 O2 on the proliferation of lung cancer cell line NCI-H1395 with low-dose 20 μm H2 O2 and after adding MEK blocking agent U0126 and Res were detected by MTS assay. The effect of H2 O2 on the phosphorylation of ERK1/2 and Akt protein and the effect of H2 O2 on the phosphorylation of MEK, ERK1/2 and c-Jun after adding Res were detected by Western Blot. Results:Low-dose H2 O2 could promote the proliferation of lung cancer cell line NCI-H1395, and H2 O2 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 H2 O2 on the proliferation of lung cancer cell line NCI-H1395 was decreased(P<0.05). Res could inhibit H2 O2 induced proliferation of lung cancer cell line NCI-H1395. After adding Res, the effects of H2 O2 on the phosphorylation of MEK, ERK1/2 and c-Jun protein were decreased(P<0.05). Conclusions: Low-dose H2 O2 can promote the proliferation of lung cancer cell line NCI-H1395, and Res can inhibit H2 O2 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.