# Investigation of the pharmacological mechanisms of Denglao Qingguan decoction in inhibiting viral pneumonia through network pharmacology and in vitro laboratory validation

**Authors:** Biao Lei, Shun Wang, Xuanxuan Li, Fang Chen, Wencong Lu, Bin Liu, Xiannan Chen, Ruihan Chen, Zhanyu Cui, Ai Li, Xi Ren, Linzhong Yu, Qinhai Ma

PMC · DOI: 10.3389/fmed.2025.1708952 · Frontiers in Medicine · 2026-01-12

## TL;DR

This study explores how Denglao Qingguan decoction fights viral pneumonia by identifying its active ingredients and testing its antiviral and anti-inflammatory effects in lab experiments.

## Contribution

The study combines network pharmacology with in vitro validation to reveal the mechanisms of a traditional herbal formula against multiple respiratory viruses.

## Key findings

- DLQGD inhibits RSV, SARS-CoV-2, and H3N2 with IC50 values of 0.4824, 1.16, and 1.592 mg/mL, respectively.
- DLQGD reduces the expression of inflammatory genes like IL6, TNF, and CXCL8 in virus-infected cells.
- DLQGD downregulates phosphorylated Stat3, Akt, and Erk1/2 proteins, indicating anti-inflammatory and antiviral pathways.

## Abstract

Respiratory viral infection poses a serious threat to human health, underscoring the need for effective agents to prevent and treat these conditions.

This study aimed to investigate Denglao Qingguan decoction (DLQGD), a traditional formula used in the management of respiratory infections, and to elucidate its efficacy and mechanisms against viral pneumonia.

Network pharmacology was employed to investigate the potential mechanism of DLQGD against viral pneumonia. The components of DLQGD were analyzed by High-Performance Liquid Chromatography-Quadrupole Time-of-Flight Mass Spectrometry (HPLC-Q-TOF MS). The antiviral effects of DLQGD against respiratory syncytial virus (RSV), influenza virus and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) were determined by cytopathic effect or MTT assays. The inhibitory effects of DLQGD on RSV or SARS-CoV-2-induced inflammatory response were determined by reverse transcriptase-quantitative PCR.

A total of 66 active ingredients were identified in DLQGD. Network pharmacology showed that DLQGD could regulate a total of 122 targets involved in viral pneumonia. The 50% inhibitory concentration (IC50) of DLQGD against RSV, SARS-CoV-2, and H3N2 was 0.4824, 1.16, and 1.592 mg/mL. The selectivity index (SI) of DLQGD against RSV, SARS-CoV-2, and H3N2 was 15.82, 5.96, and 5.74, respectively. Furthermore, DLQGD significantly inhibit the viral titer of cell culture supernatants during SARS-CoV-2 infection. DLQGD markedly reduced the mRNA expression of IL6, TNF, CXCL8, and CXCL10 in Huh-7 cells infected by SARS-CoV-2. In addition, DLQGD decreased the mRNA expression of IL6, TNF, IL1B, CXCL8, CXCL10, and CCL5 in HEp-2 cells infected by RSV. DLQGD could downregulate the protein expression of phosphorylated Stat3, Akt, and Erk1/2.

Collectively, these findings indicate that DLQGD exhibits antiviral and anti-inflammatory activities, suggesting that it could be developed into a therapeutic constituent for respiratory viral infections.

## Linked entities

- **Proteins:** STAT3 (signal transducer and activator of transcription 3), AKT1 (AKT serine/threonine kinase 1), erk1/2 (mitogen-activated protein kinase)
- **Chemicals:** IL6 (PubChem CID 165368475), TNF (PubChem CID 8521), CXCL8 (PubChem CID 74974005)
- **Diseases:** viral pneumonia (MONDO:0006012)

## Full-text entities

- **Genes:** CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CXCL10 (C-X-C motif chemokine ligand 10) [NCBI Gene 3627] {aka C7, IFI10, INP10, IP-10, SCYB10, crg-2}, CCL5 (C-C motif chemokine ligand 5) [NCBI Gene 6352] {aka D17S136E, RANTES, SCYA5, SIS-delta, SISd, TCP228}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}
- **Diseases:** inflammatory (MESH:D007249), SARS-CoV-2 infection (MESH:D000086382), respiratory infections (MESH:D012141)
- **Chemicals:** MTT (MESH:C070243), Denglao Qingguan (-)
- **Species:** H3N2 subtype (serotype) [taxon 119210], Homo sapiens (human, species) [taxon 9606], Respiratory syncytial virus (no rank) [taxon 12814], Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049]

## Full text

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## Figures

11 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12832263/full.md

## References

39 references — full list in the complete paper: https://tomesphere.com/paper/PMC12832263/full.md

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Source: https://tomesphere.com/paper/PMC12832263