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Exploring the Mechanism of Zilongjin in Treating Lung Adenocarcinoma Based on Network Pharmacology Combined with Experimental Verification  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:Exploring the Mechanism of Zilongjin in Treating Lung Adenocarcinoma Based on Network Pharmacology Combined with Experimental Verification

作者:Zhang, Kang[1];Chen, Xiaoqun[2]

机构:[1]Shaoxing Univ, Affiliated Hosp, Shaoxing Municipal Hosp, Dept Cardiothorac Surg, Shaoxing, Zhejiang, Peoples R China;[2]Shaoxing Univ, Affiliated Hosp, Shaoxing Municipal Hosp, Dept Ultrasound, 999 Zhongxing South Rd, Shaoxing 312000, Zhejiang, Peoples R China

年份:2024

卷号:44

期号:5

起止页码:27

外文期刊名:CRITICAL REVIEWS IN IMMUNOLOGY

收录:SCI-EXPANDED(收录号:WOS:001221747700003)、、WOS

基金:This work was supported by the Shaoxing Science and Technology (Grant No. 2020A13059) .

语种:英文

外文关键词:lung adenocarcinoma; Zilongjin; network pharmacology; PPAR signaling pathway; experimental verification

外文摘要:Zilongjin (ZLJ) is a common traditional Chinese medicine for lung adenocarcinoma (LUAD) treatment. However, its mechanisms of action remain to be elucidated. Network pharmacology was used to explore the underlying mechanisms of ZLJ on LUAD treatment. The disease-related targets were determined from the GeneCards and DisGeNET databases. Active compounds and targets of ZLJ were obtained from the HIT, TCMSP, and TCMID databases. Then the protein-protein interaction (PPI) network was built by the STRING database to identify core-hub targets of ZLJ in LUAD. Next, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were employed to analyze the enriched regulatory pathways of targets. Molecular docking analysis was used to evaluate interactions between potential targets and active compounds. Finally, qRT-PCR was used to further verify the results of network pharmacology. A total of 124 LUAD-related targets of ZLJ and 5 active compounds of ZLJ from the relevant databases were screened out. Among these target proteins, JUN, CDH1, PPARG, and FOS were core hub-genes in the PPI network. GO and KEGG pathway enrichment analysis indicated that these targets might regulate the PPAR signaling pathway in LUAD. JUN, PPARG, and FOS levels were upregulated, while CDH1 level was downregulated in LUAD cells. This study discerned that ZLJ may target genes such as JUN, FOS, PPARG, and CDH1 via the PPAR signaling pathway in LUAD, offering foundational insights for further exploration of ZLJ in clinical applications.

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