# Mechanistic Insights into the Therapeutic Efficacy of Qi Ling Gui Fu Prescription in Broiler Ascites Syndrome: A Network Pharmacology and Experimental Study

## TL;DR

This study investigates how Qi Ling Gui Fu Prescription treats broiler ascites syndrome by targeting vascular smooth muscle and the MAPK signaling pathway.

## Contribution

The study provides new mechanistic insights into QLGFP's therapeutic effects on broiler ascites syndrome via network pharmacology and experimental validation.

## Key findings

- QLGFP's active compounds inhibit phenotypic transformation of vascular smooth muscle in broiler ascites syndrome.
- The MAPK signaling pathway is a key target of QLGFP in treating broiler ascites syndrome.
- QLGFP reduces ascites cardiac index and suppresses MAPK pathway proteins in experimental models.

## Abstract

In this research, we explored the active components and therapeutic mechanisms of QLGFP for treating broiler AS using a network pharmacology approach. A total of 267 active compounds were isolated, of which the main active components were Dihydrokaranone, Tanshiquinone B, Neotanshinone C, etc. Bioinformatics analysis and an animal experiment indicated that the MAPK signalling pathway is the key target for QLGFP and their active compounds to improve the AS broilers by inhibiting phenotypic transformation of vascular smooth muscle. Our findings provide a scientific basis for the clinical efficacy of QLGFP in the treatment of broiler AS and a solid foundation for further elucidation of the active components and mechanism of action of QLGFP in the treatment of broiler AS.

This study delves into the therapeutic potential of Qi Ling Gui Fu Prescription (QLGFP) in broiler ascites syndrome (AS) by investigating its impact on the phenotypic transformation of vascular smooth muscle. Utilizing network pharmacology, we identified 267 active ingredients and 120 core targets of QLGFP, revealing its multifaceted mechanism of action. Gene enrichment analysis highlighted the pivotal roles of Toll-like receptor, FoxO, and MAPK signaling pathways in QLGFP’s therapeutic effects. Experimental validation in a broiler AS model demonstrated that QLGFP regulated the expression of key markers (SM-22α, OPN, and KLF4) associated with the phenotypic transformation of pulmonary artery vascular smooth muscle (PASMC). Clinical improvements were evident, with a significant reduction in ascites cardiac index (AHI). Furthermore, QLGFP suppressed the protein expression of MAPK1 (ERK1), p-MAPK1, MAPK9 (JNK2), p-MAPK9, MA3.PK14 (P38α), and p-MAPK14, along with downstream factors AP1 and ATF4. These findings suggest that QLGFP effectively prevents and treats AS in broilers by modulating the MAPKs-AP1/ATF4 pathway, thereby inhibiting the phenotypic transformation and proliferation of PASMCs. This study contributes a theoretical foundation for understanding the role of QLGFP in the prevention and treatment of AS in broilers.