Pinus koraiensis Needle Extract Attenuates Obesity-Associated Adipose and Hepatic Alterations Through Network Pharmacology

Background Obesity is a major metabolic disorder, and effective orally administrable interventions with multi-target properties are needed. Although Pinus koraiensis needles possess diverse bioactive properties, their anti-obesity effects and underlying mechanisms remain unclear. This study evaluated the anti-obesity efficacy of P. koraiensis needle extract (PKN) in vivo and explored its molecular mechanisms using integrative network pharmacology and network-based reanalysis of publicly available transcriptomic datasets. Methods Male C57BL/6J mice fed a high-fat diet (HFD) received oral PKN (80 mg/kg) for 12 weeks. Body composition, adipose histology, and hepatic lipid accumulation were assessed. Potential mechanisms were investigated by identifying overlapping genes between PKN-related compounds and obesity-associated genes, followed by protein–protein interaction network, clustering, enrichment, and transcription factor–target analyses using public transcriptomic data. Results PKN attenuated fat accumulation and epididymal adipose tissue weight in HFD-induced obese mice and reduced adipocyte hypertrophy and hepatic lipid accumulation. PKN produced a greater reduction in adipocyte diameter than Garcinia supplements. Integrative analysis identified 2619 shared target genes between PKN and obesity. As a result from clustering analysis, Cluster 4 was identified as the key hub module, and enrichment analysis highlighted cytokine response, cellular response to cytokine stimulus, and regulation of cell death. Transcription factor–target analysis suggested ILF3, HOXA10, NR3C1, and HIF1A as major putative regulators. Conclusions Orally administered PKN ameliorated obesity-associated adipose and hepatic alterations in HFD-induced obese mice. These findings suggest that PKN has anti-obesity potential and may act through a multi-target regulatory framework involving inflammation- and cell death-related pathways.