生脉散通过调控乳酸/Wnt/β-catenin/LDHA通路改善非小细胞肺癌奥希替尼耐药的作用机制

doi:10.12122/j.issn.1673-4254.2026.03.06

南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (3): 523-531.doi: 10.12122/j.issn.1673-4254.2026.03.06

• 基础研究 • 上一篇

生脉散通过调控乳酸/Wnt/β-catenin/LDHA通路改善非小细胞肺癌奥希替尼耐药的作用机制

梁芷晴¹^,³(), 潘富珍²^,⁴, 邓利强⁴, 麦哲芬⁴, 马云², 施传坚²^,⁴(), 付卫明¹^,³()

^1.南方医科大学深圳医院药学部，广东深圳 510086
^2.经方与现代中药融合创新全国重点实验室中药现代制剂技术研究中心，山东临沂 276006
^3.南方医科大学药学院，广东广州 510515
^4.广州中医药大学深圳医院（福田）肿瘤中心，广东深圳 518000

收稿日期:2025-09-11 出版日期:2026-03-20 发布日期:2026-03-26
通讯作者: 施传坚,付卫明 E-mail:liangzqing2025@163.com;shichuanjian2018@163.com;fuweiming76@smu.edu.cn
作者简介:梁芷晴，在读硕士研究生，E-mail: liangzqing2025@163.com
基金资助:
国家自然科学基金青年科学基金（C类）(82505309);中国博士后科学基金面上项目(2024M760671);广东省医学科学基金青年项目(B2025082);广州中医药大学校院联合科技创新基金-深圳医院(GZYFT2024G12);经方与现代中药融合创新全国重点实验室开放课题一般项目(LSLSKL20240118)

Shengmai San improves osimertinib resistance of non-small cell lung cancer cells by regulating the lactate/Wnt/β-catenin/LDHA pathway

Zhiqing LIANG¹^,³(), Fuzhen PAN²^,⁴, Liqiang DENG⁴, Zhefen MAI⁴, Yun MA², Chuanjian SHI²^,⁴(), Weiming FU¹^,³()

^1.Department of Pharmacy, Shenzhen Hospital, Southern Medical University, Shenzhen 510086, China
^2.State Key Laboratory of Integration and Innovation of Classic Formula and Modern Chinese Medicine, Research Center for Modern Chinese Medicine Preparation Technology, Linyi 276006, China
^3.Shool of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, China
^4.Cancer Center, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen 518000, China

Received:2025-09-11 Online:2026-03-20 Published:2026-03-26
Contact: Chuanjian SHI, Weiming FU E-mail:liangzqing2025@163.com;shichuanjian2018@163.com;fuweiming76@smu.edu.cn
Supported by:
National Natural Science Foundation of China(82505309)

摘要/Abstract

摘要：

目的探讨生脉散改善非小细胞肺癌奥希替尼耐药的作用和机制。方法制备大鼠含药血清，单用或联合奥希替尼处理人肺癌细胞A549检测细胞活力的变化，试剂盒检测细胞葡萄糖和乳酸含量变化，构建小鼠皮下肺癌模型，观察生脉散联合奥希替尼使用对奥希替尼体内抗肺癌活性的影响。Western blotting、RT-qPCR和免疫荧光实验检测生脉散和乳酸对Wnt/β-catenin/LDHA信号通路的影响。结果生脉散以浓度依赖性增加A549细胞对奥希替尼的药物敏感性，与单用奥希替尼组比较，生脉散联合奥希替尼抑制细胞活力（P<0.001），克隆形成（P<0.001）和肺癌细胞体内增长（P<0.05），生脉散呈剂量依赖性减少A549细胞葡萄糖和乳酸含量（P<0.05）。Western blotting结果显示生脉散抑制LDHA、β-catenin总蛋白、细胞质和细胞核β-catenin蛋白表达（P<0.01），而乳酸则激活β-catenin总蛋白、细胞核β-catenin和LDHA蛋白表达（P<0.001）；免疫荧光结果显示乳酸激活β-catenin蛋白核积累，而生脉散抑制细胞核β-catenin蛋白表达；RT-qPCR结果显示乳酸激活Wnt/β-catenin下游靶基因（c-myc、CD44、Axin2、Oct3/4、Survivin和CCND1）的表达（P<0.05），而生脉散则抑制其表达（P<0.05）。结论生脉散抑制肺癌细胞乳酸/Wnt/β-catenin/LDHA通路，抑制糖酵解水平，改善非小细胞肺癌奥希替尼耐药。

关键词: 生脉散, 非小细胞肺癌, 奥希替尼耐药, 糖酵解, 乳酸, 机制, Wnt/β-catenin信号通路, 乳酸脱氢酶 A

Abstract:

Objective To explore the effect of Shengmai San (SMS) for improving osimertinib resistance in non-small cell lung cancer cells and the underlying mechanism. Methods Cultured A549 cells were treated with osimertinib alone or in combination with SMS-medicated rat serum, and the changes in cell viability and glucose and lactate levels were determined. The effect of SMS combined with osimertinib for improving osimertinib resistance of A549 cells was assessed in a mouse model bearing subcutaneous A549 cell xenograft. Western blotting, RT-qPCR, and immunofluorescence staining were used to analyze the effects of SMS and lactate on the Wnt/β‑catenin/LDHA signaling pathway. Results SMS significantly increased osimertinib sensitivity of A549 cells in a concentration-dependent manner. Compared with osimertinib alone, the combined treatment with SMS and osimertinib significantly inhibited cell viability, colony formation ability, and tumor growth in nude mice. SMS concentration-dependently decreased glucose and lactate levels in A549 cells. The results of Western blotting showed that SM inhibited the protein expression of LDHA, total β‑catenin, and cytoplasmic and nuclear β‑catenin, while lactate obviously activated the expressions of total β‑catenin protein, nuclear β‑catenin, and LDHA in A549 cells. Immunofluorescence concentration-dependent staining showed that lactic acid activated nuclear accumulation of β‑catenin protein, while SMS significantly inhibited the expression of nuclear β‑catenin protein; RT-qPCR demonstrated that lactate significantly increased mRNA expressions of the Wnt/β‑catenin downstream target genes (c-myc, CD44, Axin2, Oct3/4, survivin, and CCND1), while SMS inhibited their expressions. Conclusion SMS improves osimertinib resistance in non-small cell lung cancer cells by inhibiting lactate/Wnt/β-catenin/LDHA pathway-mediated glycolysis.

Key words: Shengmai San, non-small cell lung cancer, osimertinib resistance, glycolysis, lactate, mechanism Wnt/β?catenin pathway, lactate dehydrogenase A

梁芷晴, 潘富珍, 邓利强, 麦哲芬, 马云, 施传坚, 付卫明. 生脉散通过调控乳酸/Wnt/β-catenin/LDHA通路改善非小细胞肺癌奥希替尼耐药的作用机制[J]. 南方医科大学学报, 2026, 46(3): 523-531.

Zhiqing LIANG, Fuzhen PAN, Liqiang DENG, Zhefen MAI, Yun MA, Chuanjian SHI, Weiming FU. Shengmai San improves osimertinib resistance of non-small cell lung cancer cells by regulating the lactate/Wnt/β-catenin/LDHA pathway[J]. Journal of Southern Medical University, 2026, 46(3): 523-531.

图/表 8

表1 引物序列

Tab.1 Primer sequence for RT-qPCR

Gene name		Sequence (5' to 3')
β-actin	Forward	GTCATTCCAAATATGAGATGCGT
	Reverse	GCTATCACCTCCCCTGTGTG
c-Myc	Forward	TTCGGGTAGTGGAAAACCAG
	Reverse	CAGCAGCTCGAATTTCTTCC
CD44	Forward	TCAGAGGAGTAGGAGAGAGGAAAC
	Reverse	GAAAAGTCAAAGTAACAATAACAGTGG
Axin-2	Forward	GGATCGCTCCTCTTGAAGGA
	Reverse	CTTTCGCCAACCGTGGTT
Survivin	Forward	CCACCGCATCTCTACATTCAAG
	Reverse	CAAGTCTGGCTCGTTCTCAGTG
Oct3/4	Forward	TCGAGAACCGAGTGAGAGGC
	Reverse	CACACTCGGACCACATCCTTC
Cyclin D1	Forward	CTGGAGGTCTGCGAGGAACA
Cyclin D1	Reverse	CCTTCATCTTAGAGGCCACGAA
LDHA	Forward	ATGGCAACTCTAAAGGATCAGC
LDHA	Reverse	CCAACCCCAACAACTGTAATCT

图1 549细胞存活率与克隆形成的能力

Fig.1 Viability and colony-forming ability of A549 cells with different treatments (Mean±SD, n=3). A: Viability of A549 cells treated with SMS, osimertinib, or osimertinib combined with various concentrations of SMS. B: Colony formation of A549 cells and quantitative analysis. ***P<0.001 vs Control group; #P<0.05, ##P<0.01, ###P<0.001 vs Osi group. SMS-L: SMS low-dose group; SMS-M: SMS medium-dose group; SMS-H: SMS high-dose group; Osi: Osimertinib group.

图2 动物实验体内肿瘤的相关情况

Fig.2 Assessment of xenograft growth in nude mice (Mean±SD, n=3). A-C: Representative images of xenograft tumors, growth curve and tumor weight in the tumor-bearing C57BL/6 mice in the 4 treatment groups. D: Changes in body weight of the mice in the 4 treatment groups. E: Immunohistochemistry for Ki67 in the tumor tissues in the 4 groups. *P<0.05, **P<0.01, ***P<0.001 vs Control group; #P<0.05, ###P<0.001 vs Osi group. a: Control group; b: SMS Medium-dose group; c: Osimertinib monotherapy group; d: SMS medium-dose combined with osimertinib group.

图3 各组细胞葡萄糖和乳酸浓度

Fig.3 Glucose (A) and lactate (B) concentrations A549 cells in each group (Mean±SD, n=3). *P<0.05, **P<0.01, ***P<0.001 vs Control group; ##P<0.01, ###P<0.001 vs Osi group. a: Control group; b: SMS Medium-dose group; c: Osimertinib monotherapy group; d: SMS medium-dose combined with osimertinib group.

图4 各组Wnt/β-catenin/LDHA信号通路相关蛋白和基因表达情况比较

Fig.4 Protein and mRNA expressions of the Wnt/β-catenin/LDHA signaling pathway in A549 cells in different groups (Mean±SD, n=3). A, B: Western blotting of β-catenin and LDHA expression levels in A549 cells. C: Western blotting of β-catenin expression and quantitative analysis its cytoplasmic and nuclear fractions. D: mRNA expressions of Wnt/β-catenin pathway genes detected by by RT-qPCR. *P<0.05, **P<0.01,***P<0.001 vs Control group. a: Control group; b: SMS Medium-dose group; c: Osimertinib monotherapy group; d: SMS medium-dose combined with osimertinib group.

图5 各组体内肿瘤组织中β-catenin蛋白表达比较

Fig.5 Immunohistochemistry of β-catenin protein expression in the tumor tissues in different groups (Mean±SD, n=3). **P<0.01, ***P<0.001 vs Control group;###P<0.001 vs Osimertinib group. a: Control group; b: SMS Medium-dose group; c: Osimertinib monotherapy group; d: SMS medium-dose combined with osimertinib group.

图6 各组Wnt/β-catenin/LDHA信号通路相关蛋白和基因表达情况比较

Fig.6 Expression of Wnt/β-catenin/LDHA pathway components in A549 cells with different treatments (Mean±SD, n=3). A: Western blotting of β‑catenin and LDHA expression in control and 10 mmol/L lactate-treated cells. B: Western blotting of cytoplasmic and nuclear fractions of β‑catenin in control and 10 mmol/L lactate-treated cells. C: mRNA expression of Wnt/β-catenin downstream targets detected by RT-qPCR. *P<0.05, **P<0.01, ***P<0.001 vs Control group. a: Control group; e: 10 mmol/L lactate treatment group.

图7 细胞免疫荧光检测细胞β-catenin蛋白的变化

Fig.7 Immunofluorescence staining for detecting β-catenin expression in A549 cells. A: Control group; B: SMS-Medium-dose group; C: Osimertinib monotherapy group; D: SMS medium-dose combined with osimertinib group; E: 10 mmol/L lactate treatment group.

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生脉散通过调控乳酸/Wnt/β-catenin/LDHA通路改善非小细胞肺癌奥希替尼耐药的作用机制

Shengmai San improves osimertinib resistance of non-small cell lung cancer cells by regulating the lactate/Wnt/β-catenin/LDHA pathway

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