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Objective: The objective of this study is to screen the therapeutic targets of pain of traditional Chinese medicine Chonglou and explore the relevant mechanism by network pharmacology techniques and methods. Materials and Methods: The chemical components of Chonglou were collected according to chemistry database and related literature. SwissADME was used to collect the potential active ingredients from all the chemical components of Chonglou and SwissTarget Prediction was utilized to predict their targets. The genes related to pain were collected from GeneCards and Online Mendelian Inheritance in Man databases. Joint genes were uploaded to the online string database for the analysis and the PPI network was constructed. The “Chonglou-active component-target-pain” network was constructed by Cytoscape 3.7.1 software, Gene Ontology (GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed for key target proteins. The top three active components with most targets in the network were docked with the target proteins by the molecular docking technique. Results: A total of nine potential active compounds of Chonglou, 264 potential target genes, 2385 targets of pain disorder, and 128 common targets for drug and disease were screened. One hundred and thirty-one GO items were identified by the GO enrichment analysis, and 23 related signaling pathways were identified by the KEGG pathway enrichment analysis. Molecular-docking results show that pennogenin is the optimal butt ligand of PIK3CA, STAT3, mitogen-activated protein kinase 14, and ADORA1. Conclusion: It is preliminarily revealed that Chonglou might treat pain through multiple targets, multiple biology processes and multiple pain-related signaling pathways, providing reference for the subsequent experimental research.

Background: Inflammation and oxidation stress are key factors in the mechanism of acute lung injury (ALI). Therefore, suppression of the inflammatory response and oxidative stress could be a potential strategy to treat lipopolysaccharide (LPS)-induced ALI. Ginsenoside Rd (Rd), a natural Ginseng extract, alleviates inflammation and oxidative stress in several diseases such as Alzheimer's disease and cerebral ischemia, but its effect on ALI is still unclear. Aims and Objectives: To explore the protective effect of Rd on LPS-induced ALI and explored associated mechanisms. Materials and Methods: Mice were divided into five groups: A sham-operated group, a LPS-induced ALI group, and three LPS groups pretreated with Rd doses of 20, 40, and 80 mg/kg, respectively. The pathological changes of lung, collagen deposition, pulmonary edema, inflammatory cytokine, oxidative stress and the expression levels of TLR4 and NF-κB were detected. Results: The oral administration of Rd dose dependently attenuated histopathologic changes in the lung, lung edema, pulmonary collagen deposition, protein concentration in bronchoalveolar lavage fluid (BALF), myeloperoxidase (MPO) activity, and inflammatory cell infiltration. In addition, Rd suppressed the LPS-induced inflammatory cytokines tumor necrosis factor-α, interleukin (IL)-6, and IL-1 β in BALF. The productions of oxidative stress-related enzymes (catalase, superoxide dismutase, and glutathione peroxidase) in lung tissue were significantly upregulated by Rd administration. However, malondialdehyde and pulmonary MPO activity was reduced in the Rd-pretreated groups when compared with LPS-induced ALI group. Rd treatment also dose dependently suppressed LPS-induced NF-κB activation and TLR4 expression. Conclusion: Overall, these findings provide evidence that Rd pretreatment inhibits LPS-induced ALI through anti-inflammatory and antioxidative actions, suggesting that it could be a promising protective drug for LPS-induced ALI.