| 李全志,刘志强,赵玉霞,等.榄香烯对人肺癌A549细胞系耐顺铂细胞株多药耐药的改善作用及机制研究[J].浙江中医药大学学报,2021,45(1):16-22. |
| 榄香烯对人肺癌A549细胞系耐顺铂细胞株多药耐药的改善作用及机制研究 |
| Study on the Improvement Effect and Mechanism of Elemene on Multidrug Resistance of Eisplatin-resistant Human Lung Cancer A549 Cell |
| DOI：10.16466/j.issn1005-5509.2021.01.003 |
| 中文关键词: 榄香烯 肺癌 A549/DDP细胞 多药耐药 顺铂 侵袭 凋亡 PI3K/AKT信号通路 |
| 英文关键词: elemene lung cancer A549/DDP cells multidrug resistance cisplatin invasion apoptosis PI3K/AKT signaling pathway |
| 基金项目:2017年河南省科技研发项目(152102310159) |
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| 中文摘要: |
| [目的]探究榄香烯(elemene，ELE)对顺铂(cisplatin，DDP)耐药人肺癌A549/DDP细胞系多药耐药的改善作用及其作用机制。[方法]将A549/DDP细胞分为A549/DDP组和ELE组，以四甲基偶氮唑蓝(methyl thiazolyl tetrazolium，MTT)检测24、48、72h时不同浓度ELE对A549/DDP细胞增殖能力的影响。采用DDP及20、40μg·mL-1 ELE处理A549/DDP细胞，MTT法检测ELE对细胞化疗敏感性的影响，Transwell侵袭实验检测细胞侵袭能力变化，逆转录聚合酶链式反应(reverse transcription-polymerase chain reaction，RT-PCR)检测B细胞淋巴瘤-2(B-cell lymphoma-2，Bcl-2)和Bcl-2相关X蛋白(Bcl-2-associated X，Bax)mRNA表达水平，Western blot 检测多药耐药基因1(multidrug resistance gene1，MDR1)、肺耐药相关蛋白(lung resistance-related protein，LRP)及磷脂酰肌醇-3-激酶(phosphatidy linositol-3-kinase，PI3K)/蛋白激酶B(protein kinase B，AKT)信号通路相关蛋白表达水平。[结果]MTT结果显示，ELE呈时间和剂量依赖性抑制A549/DDP细胞的增殖能力(均P＜0.05)。与单独使用DDP比较，20和40μg·mL-1 ELE提高A549/DDP细胞对DDP的敏感性，降低DDP对A549/DDP细胞的半数抑制浓度(50% inlibiting concentration，IC50)，抑制细胞的增殖能力(均P＜0.05)和侵袭能力(P＜0.05，P＜0.01)，增加细胞Bax mRNA表达水平，减少Bcl-2 mRNA表达水平(均P＜0.05)，使A549/DDP细胞MDR1、LRP、磷酸化磷脂酰肌醇-3-激酶(phosphorylated phosphatidylinositol-3-kinase，p-PI3K)和磷酸化蛋白激酶B(phosphorylated protein kinase B，p-AKT)蛋白表达水平显著降低(均P＜0.05)。[结论]ELE可增加A549/DDP细胞对DDP的敏感性，改善多药耐药现象，其作用机制可能与抑制PI3K/AKT信号通路的活化有关。 |
| 英文摘要: |
| [Objective] To investigate the improvement effect and mechanism of elemene(ELE) on the multidrug resistance of cisplatin(DDP)-resistant human lung cancer A549/DDP cell line. [Methods] A549/DDP cells were divided into A549/DDP group and ELE group. Methyl thiazolyl tetrazolium(MTT) method was used to detect the effect of ELE on proliferation of A549/DDP cells at 24， 48 and 72 h. MTT method was used to detect the effects of ELE on the sensitivity of A549/DDP cells to chemotherapy drugs. Transwell invasion test was used to detect the changes in cell invasion ability. Reverse transcription-polymerase chain reaction(RT-PCR) methods were used to detect B-cell lymphoma-2(Bcl-2) and Bcl-2-associated X(Bax) mRNA expression levels in cells. Western blot was used to detect multidrug resistance gene1(MDR1)， lung resistance-related protein(LRP) and phosphatidylinositol-3-kinase(PI3K)/protein kinase B(AKT) signaling pathway-related protein expression levels. [Results] MTT test results showed that ELE inhibited the proliferation of A549/DDP cells in a time and dose-dependent manner(all P＜0.05). Compared with DDP alone， 20 and 40μg·mL-1 ELE increased the sensitivity of A549/DDP cells to DDP， decreased the 50% inhibiting concentration(IC50) of DDP to A549/DDP cells， and inhibited cell proliferation(all P＜0.05) and invasion ability(P＜0.05， P＜0.01)， increased the expression level of Bax mRNA， decreased the expression level of Bcl-2 mRNA(all P＜0.05)， and significantly reduced the expression levels of MDR1， LRP， phosphorylated phosphatidylinositol-3-kinase(p-PI3K) and phosphorylated protein kinase B(p-AKT) protein in A549/DDP cells(all P＜0.05). [Conclusion] ELE can increase the sensitivity of A549/DDP cells to DDP and improve multidrug resistance. Its mechanism of action may be related to inhibiting the activation of PI3K/AKT signaling pathway. |
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