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李纪鹏,陈丽萍,俞万钧.白花蛇舌草乙醇提取物逆转肺癌细胞化疗耐药的作用研究[J].浙江中西医结合杂志,2020,30(7):
白花蛇舌草乙醇提取物逆转肺癌细胞化疗耐药的作用研究
Effect of ethanol extract from Hedyotis diffusa on chemotherapy resistance of lung cancer cells
投稿时间:2020-01-12  修订日期:2020-04-24
DOI:
中文关键词:  白花蛇舌草  上皮间质转化  化疗耐药  PI3K/Akt信号通路
英文关键词:Hedyotis diffusa willd  epithelial-mesenchymal transition  Chemotherapy resistance  PI3K/Akt signaling pathway
基金项目:浙江省中医药科技计划项目(No. 2017ZA128) 通讯作者:俞万钧,Tel: 0574-87017390;E-mail:nbyuwanjun@163.com
作者单位E-mail
李纪鹏 宁波市鄞州人民医院 lijipeng1109@163.com 
陈丽萍 宁波市鄞州人民医院  
俞万钧 宁波市鄞州人民医院 nbyuwanjun@163.com 
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中文摘要:
      摘 要 目的 探讨白花蛇舌草乙醇提取物(EEHDW)在肺癌化疗耐药中的作用及可能的机制。方法 EEHDW作用于多西他赛耐药细胞系A549/DTX后,采用集落形成、Transwell和CCK-8检测处理前后细胞的增殖、侵袭和半数抑制量(IC50)情况,Western blot检测上皮间质转化相关蛋白E-钙黏蛋白(E-cadherin)和波形蛋白(vimentin)的表达,同时分析PI3K/Akt信号通路中磷酸化PI3K(p-PI3K)和磷酸化Akt(p-Akt)蛋白表达变化情况。结果 与亲本A549细胞相比,多西他赛耐药的A549/DTX发生了上皮间质转化(EMT);与对照组相比,EEHDW(2、4、6mg/mL)能抑制A549/DTX细胞的集落形成[(102±9.23)、(69±4.25)、(68±3.12)比(201±8.18), P<0.05]和侵袭能力[(42±5.58)、(21±3.25)、(22±4.36)比(129±9.23), P<0.05];Western blot结果显示EEHDW(2mg/mL)能够上调E-cadherin蛋白表达,下调vimentin蛋白表达[(31.35±5.27)比(76.05±7.81)、(82.24±6.80)比(35.04±5.32),P<0.05];EEHDW(2mg/mL)处理A549/DTX细胞48h后,细胞对多西他赛的半数抑制量IC50显著降低[(81.36±7.58)比(45.38±6.82) ,P<0.05];此外,与对照组相比,EEHDW(2mg/mL)能够抑制磷酸化(p)-PI3K[(45.62±6.15)比(22.85±4.29) ,P<0.05]和p-Akt[(43.51±3.18)比(23.25±3.67) ,P<0.05]蛋白的表达水平。结论 EEHDW能够抑制A549/DTX细胞增殖、侵袭,逆转多西他赛诱导的EMT和化疗耐药,其机制可能与PI3K/Akt信号通路有关。
英文摘要:
      ABSTRACT Objective To to explore the role and possible mechanism of ethanol extract of HDW(EEHDW) in chemotherapy resistance of lung cancer. Methods The docetaxel resistant cell line A549/DTX was established in vitro. After treatment of A549/DTX with EEHDW, the proliferation, invasion and the 50% inhibition concentration (IC50) value of cells were detected by colony formation assay, Transwell assay and CCK-8 assay. The expression of epithelial-mesenchymal transition-related protein E-cadherin and vimentin were determined by western blot. In addition, the phosphorylated PI3K (p-PI3K) and phosphorylated Akt (p-Akt) protein expression in PI3K/Akt signaling pathway were aslo analysed. Results Docetaxe-resistant A549/DTX underwent EMT in comparison with parent A549 cells. compared with the control group, EEHDW (2, 4, 6 mg/mL) can inhibit A549/DTX cell colony formation [(102 ± 9.23), (69 ± 4.25), (68 ± 3.12) vs (201 ± 8.18), P <0.05] and invasive capacity [(42 ± 5.58), (21 ± 3.25) (22 ± 4.36) vs (129 ± 9.23), P <0.05]; Western blot results showed that EEHDW (2mg/mL)can up-regulate E-cadherin protein expression and down-regulate vimentin protein expression [(31.35 ± 5.27) vs (76.05 ± 7.81), (82.24) ± 6.80) vs (35.04 ± 5.32), P <0.05]; After the A549/DTX cells were treated with EEHDW (2mg/mL) for 48h, the IC50 of half-inhibition of docetaxel was significantly reduced [(81.36 ± 7.58) vs (45.38 ± 6.82), P <0.05]; In addition, compared with the control group, EEHDW (2mg/mL) was able to inhibit phosphorylation (p) -PI3K [(45.62 ± 6.15) vs (22.85 ± 4.29), P <0.05] and p-Akt [(43.51 ± 3.18) vs (23.25 ± 3.67), P <0.05] protein expression level. Conclusion EEHDW can inhibit the proliferation and invasion of A549/DTX cells and reverse the docetaxel-induced EMT and chemotherapy resistance. The mechanism may be related to PI3K/Akt signaling pathway.
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