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清肺化瘀解毒方对非小细胞肺癌细胞耐药的逆转作用研究
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| 篇名： | 清肺化瘀解毒方对非小细胞肺癌细胞耐药的逆转作用研究 |
| TITLE： | Study on the reversal effect of Qingfei huayu jiedu formula on drug resistance in non-small cell lung cancer cells |
| 摘要： | 目的 基于微RNA-641（miR-641）/胞外信号调节激酶（ERK）信号通路，探讨清肺化瘀解毒方（QFHYJDF）对非小细胞肺癌（NSCLC）细胞耐药的逆转作用。方法以人NSCLC亲本细胞A549为对象，采用浓度梯度递增联合高浓度冲击策略构建吉非替尼耐药细胞系A549/GR。在筛选干预浓度及时间后，将耐药细胞分为对照血清组（20%空白血清作用48h）、QFHYJDF含药血清组（20%QFHYJDF含药血清作用48h）和常规培养组（常规培养48h），检测各组细胞的相对活力和总凋亡率，以及细胞中miR-641和神经纤维蛋白1（NF1）、ERK1/2、磷酸化ERK1/2（p-ERK1/2）的表达水平。结果与常规培养组和对照血清组比较，QFHYJDF含药血清组细胞的相对活力均显著降低，总凋亡率均显著升高，细胞中NF1蛋白的表达均显著上调，miR-641和p-ERK1、p-ERK2蛋白的表达均显著下调（P＜0.05）。结论QFHYJDF可抑制吉非替尼耐药肺癌细胞的增殖，促进其凋亡，上述作用可能与上调NF1蛋白表达、抑制miR-641表达及ERK信号通路活性有关。 |
| ABSTRACT： | OBJECTIVE To investigate the reversal effect of Qingfei huayu jiedu formula （QFHYJDF） on drug resistance in non-small cell lung cancer （NSCLC） cells based on the microRNA-641 （miR-641）/extracellular signal-regulated kinase （ERK） signaling pathway. METHODS The human parental NSCLC cell line A549 was used to establish gefitinib-resistant cells A549/GR by combining concentration gradient increment with high-concentration pulse strategy. After screening for optimal intervention concentration and duration， the resistant cells were divided into a control serum group （treated with 20% blank serum for 48 h）， QFHYJDF-containing serum group （treated with 20% QFHYJDF-containing serum for 48 h）， and the normally cultured group （normally cultured for 48 h）. The cell relative viability， total apoptosis rate， as well as the expression levels of miR-641， neurofibromin 1 （NF1）， ERK1/2， and phosphorylated ERK1/2 （p-ERK1/2）， were assessed in each group. RESULTS Compared with the normally cultured group and the control serum group， the QFHYJDF-containing serum group exhibited significantly decreased cell relative viability and significantly increased total apoptosis rate （ P ＜0.05）. Moreover， the expression of NF1 protein was significantly up-regulated， while the expression levels of miR-641 and p-ERK1， p-ERK2 proteins were significantly down-regulated in the QFHYJDF-containing serum group （ P ＜0.05）. CONCLUSIONS QFHYJDF can inhibit proliferation and promote apoptosis of gefitinib-resistant lung cancer cells， which may be associated with up-regulating NF1 protein expression， down-regulating miR-641 expression， and inhibiting the activity of the ERK signaling pathway. |
| 期刊： | 2026年第37卷第12期 |
| 作者： | 陈帅龙；刘慧慧；桑锋；蒋立峰 |
| AUTHORS： | CHEN Shuailong，LIU Huihui，SANG Feng，JIANG Lifeng |
| 关键字： | 清肺化瘀解毒方; 非小细胞肺癌; 吉非替尼耐药; miR-641/ERK信号通路 |
| KEYWORDS： | Qingfei huayu jiedu formula; non-small cell lung cancer; gefitinib resistance; miR-641/ERK signaling pathway |
| 阅读数： | 1 次 |
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