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1.河南中医药大学第一附属医院血液肿瘤科,郑州 450003
2.中西医防治重大疾病河南省协同创新中心,郑州 450003
3.河南中医药大学第一附属医院艾滋病临床研究中心,郑州 450003
4.河南省肿瘤医院中西医结合科,郑州 450008
硕士研究生。研究方向:中西医结合防治恶性肿瘤。E-mail:1744131172@qq.com
副主任医师,硕士生导师,博士。研究方向:中西医结合防治恶性肿瘤。E-mail:Jlf_2000@126.com
收稿:2025-12-14,
修回:2026-04-14,
录用:2026-05-19,
纸质出版:2026-06-30
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陈帅龙,刘慧慧,桑锋,等.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[J].中国药房,2026,37(12):1553-1558.
CHEN Shuailong,LIU Huihui,SANG Feng,et al.Study on the reversal effect of Qingfei huayu jiedu formula on drug resistance in non-small cell lung cancer cells[J].ZHONGGUO YAOFANG,2026,37(12):1553-1558.
陈帅龙,刘慧慧,桑锋,等.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[J].中国药房,2026,37(12):1553-1558. DOI: 10.6039/j.issn.1001-0408.2026.12.06.
CHEN Shuailong,LIU Huihui,SANG Feng,et al.Study on the reversal effect of Qingfei huayu jiedu formula on drug resistance in non-small cell lung cancer cells[J].ZHONGGUO YAOFANG,2026,37(12):1553-1558. DOI: 10.6039/j.issn.1001-0408.2026.12.06.
目的
2
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
2
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48 h)、QFHYJDF含药血清组(20%QFHYJDF含药血清作用48 h)和常规培养组(常规培养48 h),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
2
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
2
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。
OBJECTIVE
2
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
2
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
2
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
2
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.
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