Kangliu Zengxiao Jiandu Prescription in Enhancing Cisplatin Chemotherapy for Lung Cancer:A Network Pharmacology and Experimental Study
10.19879/j.cnki.1005-5304.202502232
- VernacularTitle:抗瘤增效减毒方增强肺癌顺铂化疗疗效的网络药理学及实验研究
- Author:
Wenjie WANG
1
;
Xin LIU
1
;
Jia YANG
1
;
Xiaojie FU
1
;
Xinhong WU
1
;
Yuejiao CAI
1
;
Zhenye XU
1
;
Zhongqi WANG
1
;
Haibin DENG
1
Author Information
1. 上海中医药大学附属龙华医院,上海 200030
- Publication Type:Journal Article
- Keywords:
combination therapy;
Kangliu Zengxiao Jiandu Prescription;
lung cancer;
network pharmacology;
EGFR/PI3K/AKT pathway
- From:
Chinese Journal of Information on Traditional Chinese Medicine
2025;32(8):38-45
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the mechanism of Kangliu Zengxiao Jiandu Prescription(KLJD)in enhancing the efficacy of cisplatin chemotherapy in non-small cell lung cancer(NSCLC)through network pharmacology and in vivo/in vitro experiments.Methods Components of KLJD were screened via the TCMSP database to identify active components and potential targets.Lung cancer-related genes were obtained from the GeneCards and OMIM databases.GO and KEGG pathway enrichment analysis was performed on drug-disease intersection targets using the Metascape database;molecular docking was performed between core target proteins and main active components.A Lewis lung cancer mouse model was established,and intervened with KLJD and cisplatin.Organ indexes and tumor inhibition rate were counted,and Western blot and RT-PCR were used to detect the expressions of key pathway target proteins and mRNA;A549 and H1299 cells were intervened with KLJD,and Western blot was used to detect key target protein expressions.Results Network pharmacology identified 74 active components and 20 key targets of KLJD,primarily involved in biological processes such as cell proliferation and inflammatory response,and pathways in cancer and PI3K/AKT signaling pathway;molecular docking revealed stable binding between EGFR and major compounds.Animal experiments demonstrated that,compared with the model group,the KLJD group showed significantly higher tumor inhibition rate(P<0.01)and downregulation of EGFR,AKT and PI3K protein and mRNA expression in tumor tissues(P<0.05).Compared with the cisplatin group,the combination group exhibited significantly enhanced tumor inhibition rate(P<0.01),elevated thymic and splenic indices(P<0.01),and decreased EGFR,PI3K and AKT protein and mRNA expressions(P<0.01).Cell experiments showed that KLJD concentration-dependently inhibited A549 and H1299 cell proliferation(IC50:14.72 mg/mL and 14.68 mg/mL,respectively).Combined with cisplatin,KLJD synergistically down-regulated EGFR PI3K and AKT protein expressions(P<0.01).Conclusion KLJD effectively enhances cisplatin's chemotherapeutic efficacy in NSCLC by inhibiting the EGFR/PI3K/AKT pathway while improving immune organ function.Its mechanism likely involves multi-target regulation,including suppression of tumor proliferation,promotion of apoptosis,and modulation of the immune microenvironment.
