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

Abstract

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.

Keywords

• network pharmacology
• Qi Ling Gui Fu prescription
• broiler ascites syndrome
• MAPK pathway
• phenotypic switching of VSMC