Background/Objectives: Moschus (musk) has long been used in traditional Tibetan medicine to prevent and treat epidemic febrile illnesses. However, its antiviral mechanisms remain poorly understood. Given the urgent need for effective treatments against viral respiratory tract infections (VRTIs), this study aimed to systematically investigate the molecular targets and pharmacological pathways through which Moschus may exert therapeutic effects. Methods: Based on the identification of bioactive compounds with favorable pharmacokinetics, we applied integrated network pharmacology and multi-omics analyses to systematically identify key therapeutic targets involved in VRTIs. Gene Set Enrichment Analysis (GSEA) and immune infiltration further revealed strong associations with multiple immune cell subsets, reflecting their pivotal roles in immunomodulatory mechanisms during viral infections. Molecular docking confirmed the strong binding affinities between Moschus compounds and these key targets. Results: Notably, testosterone exhibited the strongest and most consistent binding across key targets, suggesting its potential as a pivotal bioactive compound. Importantly, the antiviral effects of Moschus may be mediated in part by the downregulation of the key genes MCL1, MAPK3, and CDK2, which are involved in the regulation of viral replication, apoptosis, and host immune responses. Conclusions: This study provides a comprehensive mechanistic framework supporting the multi-target antiviral potential of Moschus, offering a scientific basis for its further development as a therapeutic agent against VRTIs.

Acorus calamus, a traditional Tibetan medicine with potential antiviral activity but undefined mechanisms, was studied for its anti-respiratory syncytial virus (RSV) mechanisms using network pharmacology and molecular docking, given RSV’s substantial disease burden and lack of specific therapies. The primary active compounds were identified and analyzed through a literature search, the PubChem database, and the SwissADME. Relevant targets were sifted through the SwissTargetPrediction platform, OMIM, and GeneCards databases. Common targets underwent enrichment analysis using Disease Ontology (DO), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG). Molecular docking and GEO datasets were used for further analysis. Among the screened data, 268 targets were associated with Acorus calamus compounds and 1633 with RSV. KEGG analysis of the shared targets revealed potential therapeutic roles via the PI3K–Akt and JAK–STAT signaling pathways. Molecular docking results demonstrated that CCND1, EGFR, and SRC exhibited relatively lower binding energies with compounds in comparison to other proteins, suggesting better interactions, and GEO-derived RSV datasets further validated CCND1’s significance. This study demonstrates Acorus calamus’s anti-RSV activity and its potential mechanism, providing a theoretical foundation for the effective active ingredients of Acorus calamus targeting CCND1 as a strategy to combat RSV infection.

Background: Kaempferol (Kae), a flavonoid compound, has shown considerable potential in preventing and treating cardiovascular diseases and ameliorating myocardial damage. However, its underlying mechanisms remain complex and require further elucidation. This study investigated the protective effects of Kae pretreatment against lipopolysaccharide (LPS)-induced inflammatory responses in H9c2 cardiomyocytes through the interleukin-6 (IL-6)/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway, aiming to establish a theoretical foundation for Kae development and clinical application. Methods: Initially, potential targets were identified through network pharmacology and molecular docking. The protective efficacy of Kae against CS was then preliminarily validated in vivo via histopathological analysis (hematoxylin and eosin staining). Finally, an LPS-induced CS model was constructed in H9c2 cardiomyocytes to elucidate the underlying mechanisms in vitro. Results: Network pharmacology analysis indicated that Kae may exert anti-CS effects via modulation of the IL-6/JAK2/STAT3 signaling pathway. In vivo experiments demonstrated that Kae significantly ameliorated histopathological changes, including disorganized myocardial fibers and inflammatory cell infiltration. Compared with the model group, serum levels of tumor necrosis factor alpha (TNF-α), IL-6, and interleukin-1β (IL-1β) were significantly decreased, along with reduced mRNA expression of these cytokines in cardiac tissue. In vitro, LPS stimulation significantly elevated the levels of TNF-α, IL-6, and IL-1β, and increased phosphorylated Janus kinase 2 (p-JAK2) and phosphorylated signal transducer and activator of transcription 3 (p-STAT3) expression compared with the control group ( P < 0.01). Kae pretreatment significantly reduced these inflammatory mediators and downregulated p-JAK2 and p-STAT3 expression compared with the LPS group ( P < 0.01). Additionally, Kae pretreatment increased superoxide dismutase activity while decreasing malondialdehyde content and nitric oxide production ( P < 0.05). Conclusion: Kae pretreatment demonstrated a protective effect against the LPS-induced inflammatory response in H9c2 cells. This protective effect potentially involves regulating the IL-6/JAK2/STAT3 signaling pathway.