文章摘要
隗玉川,程万宏,应朝辉,于 林,王艳俊.槐耳清膏抑制非小细胞肺癌细胞增殖和血管新生的作用机制研究[J].,2022,(2):226-229
槐耳清膏抑制非小细胞肺癌细胞增殖和血管新生的作用机制研究
Mechanism of Huaier on Inhibiting Proliferation and Angiogenesis of Non-Small Cell Lung Cancer Cells
投稿时间:2021-05-24  修订日期:2021-06-21
DOI:10.13241/j.cnki.pmb.2022.02.005
中文关键词: 槐耳清膏  非小细胞肺癌  EGFR  VEGFR2  细胞增殖  血管新生
英文关键词: Huaier  Non-small cell lung cancer  EGFR  VEGFR2  Cell proliferation  Angiogenesis
基金项目:辽宁省自然科学基金指导计划项目(20170318)
作者单位E-mail
隗玉川 大连大学附属新华医院胸外科 辽宁 大连 116023 kych9561@163.com 
程万宏 大连大学附属新华医院胸外科 辽宁 大连 116023  
应朝辉 大连大学附属新华医院胸外科 辽宁 大连 116023  
于 林 大连大学附属新华医院胸外科 辽宁 大连 116023  
王艳俊 大连大学附属新华医院胸外科 辽宁 大连 116023  
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中文摘要:
      摘要 目的:探讨槐耳清膏抑制非小细胞肺癌(NSCLC)细胞增殖和血管新生的作用机制。方法:选择对数生长期的NSCLC细胞,经过传代培养成细胞株后采用随机法分成低剂量组、高剂量组以及空白对照组。其中低剂量组和高剂量组分别加入5 μmol/L、10 μmol/L的槐耳清膏进行处理,而空白对照组未加入槐耳清膏处理。利用细胞增殖毒性试验法(MTT)检测NSCLC细胞的存活率,并采用蛋白免疫印迹实验(WB)法检测表皮生长因子受体(EGFR)和血管内皮生长因子受体2(VEGFR2)、磷酸化EGFR(pEGFR)、磷酸化VEGFR2(pVEGFR2)、磷脂酰肌醇3-激酶(PI3K)、磷酸化丝氨酸/苏氨酸特异性蛋白激酶(pAKT)(pAKT)、磷酸化细胞外信号调节激酶1/2(pERK1/2)、磷酸化应激活化蛋白激酶1/2(pJNK1/2)、磷酸化-p38(pp38)、细胞周期蛋白D1(Cyclin D1)及增殖细胞核抗原(PCNA)蛋白表达水平。结果:低剂量组、高剂量组NSCLC细胞的存活率均显著低于空白对照组(P<0.05)。与空白对照组相比,槐耳清膏处理NSCLC细胞后,低剂量组、高剂量组中pEGFR、pVEGFR2蛋白的相对表达水平均显著降低(P<0.05)。与空白对照组比较,槐耳清膏处理NSCLC细胞后,低剂量组、高剂量组中PI3K蛋白、pAKT、pERK1/2、pJNK1/2、pp38、Cyclin D1及PCNA的相对表达水平均显著降低(P<0.05)。结论:基于EGFR/VEGFR2信号通路,槐耳清膏对NSCLC细胞增殖和血管新生有一定的抑制作用,可能成为一种针对NSCLC的有用靶向药物。
英文摘要:
      ABSTRACT Objective: To investigate the mechanism of huaier on inhibiting proliferation and angiogenesis of non-small cell lung cancer (NSCLC). Methods: The NSCLC cells in the logarithmic growth phase were selected, subcultured into cell lines and then randomly divided into low-dose group, high-dose group and blank control group. Among them, the low-dose group and the high-dose group were treated with 5 μmol/L and 10 μmol/L huaier, respectively, while the blank control group was not treated with huaier. The cell proliferation toxicity test(MTT) was used to detect the survival rate of NSCLC cells, and the Western blotting(WB) method was used to detect epidermal growth factor receptor (EGFR), vascular endothelial growth factor receptor 2 (VEGFR2), and phosphorylated EGFR (pEGFR), phosphorylated VEGFR2(pVEGFR2), phosphatidylinositol 3-kinase(PI3K), phosphorylated A(pAKT), phosphorylated ERK1/2(pERK1/2), phosphorylated JNK1/2(pJNK1/2), phosphorylated p38 (pp38), cyclin D1 (Cyclin D1) and proliferating cell nuclear antigen (PCNA) protein expression levels. Results: The survival rate of NSCLC cells in the low-dose and high-dose groups was significantly lower than that of the blank control group(P<0.05). Compared with the blank control group, after Huaier treated NSCLC cells, the relative expression levels of pEGFR and pVEGFR2 protein in the low-dose and high-dose groups were significantly reduced(P<0.05). Compared with the blank control group, the relative expression levels of PI3K protein, pAKT, pERK1/2, pJNK1/2, pp38, Cyclin D1 and PCNA in the low-dose group and high-dose group were significantly reduced after treating NSCLC cells with Huaier(P<0.05). Conclusion: Based on the EGFR/VEGFR2 signaling pathway, Huaier has a certain inhibitory effect on NSCLC cell proliferation and angiogenesis, and may become a useful targeted drug for NSCLC.
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