Exploring the mechanism of artemisinin in alleviating lung injury caused by cardiac arrest and cardiopulmonary resuscitation based on network pharmacology and molecular docking technology

Objective: To elucidate the mechanisms through which artemisinin mitigates lung injury post-cardiac arrest and cardiopulmonary resuscitation (CA-CPR), this study applies network pharmacology and molecular docking techniques. Methods: Target proteins for artemisinin were pinpointed using the TCM System Pharmacology Database and Analysis Platform, the Herb Database, and GeneCards. Predictive analyses for lung injury-related targets post-CA-CPR were conducted through GeneCards, with intersections analyzed to identify shared targets. The STRING Database was utilized to create a protein-protein interaction (PPI) network, and core targets were determined using Cytoscape 3.7.2 software. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed via the Weisenxin online mapping website, while molecular docking was executed with Autodock Vina 1.1.2, and visualization was achieved using PyMOL 2.1 software. Results: A total of 202 artemisinin targets, 7348 disease targets, 195 intersecting targets, and 21 core targets were identified. GO analysis revealed 78 cell components, 2873 biological processes, and 186 molecular functions. KEGG analysis highlighted involvement in pathways such as PI3K-Akt, AGE-RAGE, apoptosis, and TNF. Molecular docking results indicated strong binding activity of artemisinin with the core targets. Conclusion: Artemisinin may mitigate lung injury following cardiac arrest and cardiopulmonary resuscitation through various pathways and targets, suggesting new avenues for further basic and clinical research.