# Qingfei Formula Protects against Human Respiratory Syncytial Virus-induced Lung Inflammatory Injury by Regulating the MAPK Signaling Pathway

**Authors:** Ya-Lei Sun, Pei-Pei Zhao, Cheng-Bi Zhu, Xin-Min Li, Bin Yuan

PMC · DOI: 10.2174/1386207326666230821121358 · 2024-04-26

## TL;DR

Qingfei formula reduces lung inflammation caused by respiratory syncytial virus by targeting the MAPK signaling pathway.

## Contribution

This study reveals the mechanism by which Qingfei formula protects against RSV-induced lung injury through the MAPK pathway.

## Key findings

- Qingfei formula downregulated the MAPK signaling pathway in RSV-infected mice.
- The formula reduced inflammatory mediators like IL-6, IL-8, and P-STAT3 in infected mice.
- Molecular docking confirmed stable binding of QF ingredients to genes in the MAPK pathway.

## Abstract

Qingfei formula (QF) is an empirical formula that shows good clinical efficacy in treating human respiratory syncytial virus pneumonia (RSVP). However, the underlying mechanism remains unclear. This study explores the possible pharmacological actions of QF in RSVP treatment.

We used a network pharmacology approach to identify the active ingredients of QF, forecast possible therapeutic targets, and analyze biological processes and pathways. Molecular docking simulation was used to evaluate the binding capability of active ingredients and therapeutic targets. Finally, in vivo experiments confirmed the reliability of network pharmacology-based prediction of underlying mechanisms.

The study identified 92 potential therapeutic targets and corresponding 131 active ingredients. Enrichment analysis showed that QF downregulated the MAPK signaling pathway and suppressed the inflammatory injury to the lungs induced by the RSV virus. Molecular docking simulations demonstrated that the core active ingredients of QF could stably bind to genes associated with the MAPK signaling pathway. QF had a protective effect against pneumonia in RSV-infected mice. The QF group exhibited a significant reduction in the levels of inflammatory mediators, interleukin-6 (IL-6), interleukin-8 (CXCL8, IL-8), and P-STAT3, compared to the RSV-induced group. The QF group showed remarkably inhibited MAPK1+3(P-ERK1+2) and MAPK8(P-JNK) protein expression.

The current study showed that QF downregulated the MAPK signaling pathway, which inhibited pulmonary inflammation triggered by RSV infection. This study recommends the appropriate use of QF in the clinical management of RSVP.

## Linked entities

- **Genes:** MAPK1 (mitogen-activated protein kinase 1) [NCBI Gene 5594], MAPK3 (mitogen-activated protein kinase 3) [NCBI Gene 5595], MAPK8 (mitogen-activated protein kinase 8) [NCBI Gene 5599], STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774]
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}, ERK1+2 [NCBI Gene 26417;26413], MAPK1+3 [NCBI Gene 26415;26413;26417], Cxcl15 (C-X-C motif chemokine ligand 15) [NCBI Gene 20309] {aka Il8, Scyb15, lungkine, weche}, Stat3 (signal transducer and activator of transcription 3) [NCBI Gene 20848] {aka 1110034C02Rik, Aprf}, Mapk8 (mitogen-activated protein kinase 8) [NCBI Gene 26419] {aka JNK, JNK1, Prkm8, SAPK1}
- **Diseases:** Lung Inflammatory Injury (MESH:D055370), RSVP (MESH:D011014), inflammatory (MESH:D007249), lungs (MESH:D008171)
- **Chemicals:** Qingfei (-)

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11165710/full.md

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Source: https://tomesphere.com/paper/PMC11165710