Related Experiment Video
Updated: May 12, 2026
Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma
Published on: March 3, 2023
Chlorogenic acid attenuates idiopathic pulmonary fibrosis: An integrated analysis of network pharmacology, molecular
Juan Manuel Velázquez-Enríquez1, Jovito Cesar Santos-Álvarez1, Alma Aurora Ramírez-Hernández1
1Laboratorio de Fibrosis y Cáncer, Facultad de Medicina y Cirugía, Universidad Autónoma Benito Juárez de Oaxaca, Ex Hacienda de Aguilera S/N, Sur, San Felipe del Agua, Oaxaca, C.P. 68020, Mexico.
Aims:
Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive lung condition, the cause of which remains unknown and for which no effective therapeutic treatment is currently available. Chlorogenic acid (CGA), a natural polyphenolic compound found in different plants and foods, has emerged as a promising agent due to its anti-inflammatory, antioxidant, and antifibrotic properties. However, the molecular mechanisms underlying the therapeutic effect of CGA in IPF remain unclear. The purpose of this study was to analyze the pharmacological impact and underlying mechanisms of CGA in IPF.
Main Methods:
Using network pharmacology analysis, genes associated with IPF and potential molecular targets of CGA were identified through specialized databases, and a protein-protein interaction (PPI) network was constructed. Molecular docking was performed to accurately select potential therapeutic targets. To investigate the effects of CGA on lung histology and key gene expression, a murine model of bleomycin-induced lung fibrosis was used.
Key Findings:
Network pharmacology analysis identified 384 were overlapped between CGA and IPF. Key targets including AKT1, TP53, JUN, CASP3, BCL2, MMP9, NFKB1, EGFR, HIF1A, and IL1B were identified. Pathway analysis suggested the involvement of cancer, atherosclerosis, and inflammatory processes. Molecular docking confirmed the stable binding between CGA and targets. CGA regulated the expression mRNA of EGFR, MMP9, AKT1, BCL2 and IL1B and attenuated pulmonary fibrosis in the mouse model.
Significance:
CGA is a promising multi-target therapeutic agent for IPF, which is supported by its efficacy in reducing fibrosis through the modulation of key pathways. This evidence provides a basis to further investigate CGA as an IPF potential treatment.
Insights
Chlorogenic acid (CGA) shows potential in treating idiopathic pulmonary fibrosis (IPF) by modulating key molecular pathways. This study investigated CGA
Area of Science:
- Pharmacology
- Molecular Biology
- Pulmonology
Background:
- Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with unknown causes and no effective treatments.
- Chlorogenic acid (CGA), a natural compound, exhibits anti-inflammatory, antioxidant, and antifibrotic properties, suggesting therapeutic potential for IPF.
- The precise molecular mechanisms of CGA's action in IPF require elucidation.
Purpose of the Study:
- To analyze the pharmacological effects of Chlorogenic acid (CGA) on idiopathic pulmonary fibrosis (IPF).
- To investigate the underlying molecular mechanisms of CGA's therapeutic action in IPF.
Main Methods:
- Network pharmacology was employed to identify IPF-associated genes and potential CGA targets, constructing a protein-protein interaction (PPI) network.
- Molecular docking was utilized to validate the binding affinity of CGA to selected therapeutic targets.
- A bleomycin-induced murine model of lung fibrosis was used to assess CGA's effects on lung histology and gene expression.
Main Results:
- Network pharmacology identified 384 overlapping targets between CGA and IPF, highlighting key genes such as AKT1, TP53, and EGFR.
- Pathway analysis indicated involvement in cancer, atherosclerosis, and inflammatory processes, with molecular docking confirming stable CGA-target binding.
- CGA treatment modulated mRNA expression of EGFR, MMP9, AKT1, BCL2, and IL1B, and significantly attenuated pulmonary fibrosis in the mouse model.
Conclusions:
- Chlorogenic acid (CGA) demonstrates multi-target therapeutic potential for idiopathic pulmonary fibrosis (IPF).
- CGA effectively reduces fibrosis by modulating critical molecular pathways, supporting its investigation as a potential IPF treatment.
More Related Videos
Related Concept Videos
01:20Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation
01:23Chronic Obstructive Pulmonary Disease II: Emphysema
01:24Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features