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  3. Quercetin attenuates deoxynivalenol-induced muscle developmental disorders in broilers by modulating the PI3K/Akt/mTOR pathway and reducing apoptosis

Quercetin attenuates deoxynivalenol-induced muscle developmental disorders in broilers by modulating the PI3K/Akt/mTOR pathway and reducing apoptosis

  • Poult Sci. 2026 Jun;105(6):106740. doi: 10.1016/j.psj.2026.106740.
Yi Fang 1,  Hongyu Fu 1,  Xuehan Jiang 1,  Hongxue Yang 1,  Yishan Yin 1,  Bo Li 1,  Xiaoxiao Chen 1,  Bendong Shi 1,  Jingzeng Cai 1,  Ziwei Zhang 2
Affiliations

Affiliations

  • 1 College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
  • 2 College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China. Electronic address: [email protected].
PMID: 41850073 DOI: 10.1016/j.psj.2026.106740
Abstract

Deoxynivalenol (DON), as the most prevalent mycotoxin, not only poses a significant threat to animal and human health but also exerts pronounced adverse effects on growth and development. Quercetin (QUE), a naturally occurring antioxidant, is known to promote muscle growth and differentiation. In this study, a DON-exposed broiler model with QUE intervention was established to investigate the protective mechanisms of QUE against DON-induced skeletal muscle toxicity. Eighty broilers were randomly divided into four groups: CON group, DON group, QUE group, and DON+QUE group. Each group received oral administration of 10 mg/kg DON and/or 4 mg/kg QUE. For in vitro experiments, myoblasts were used as experimental subjects to establish intervention models with LY294002, Z-VAD-FMK, and IBS008738. This study demonstrates that DON exposure induces oxidative stress and Apoptosis (increased by 329%) in both in vivo muscle tissue and in vitro myoblasts, inhibits the expression of myogenic regulatory factors such as MYH2, and consequently leads to structural muscle damage and developmental impairment. Crucially, we identified that QUE effectively alleviated DON-induced oxidative stress (CAT activity increased by 45.1%), Apoptosis (nearly completely inhibited), and muscle developmental disorders (MYH2 increased by 35.2%) by upregulating the transcription and phosphoprotein expression levels of genes associated with the PI3K/Akt/mTOR signaling pathway. The pivotal role of this pathway was further confirmed by the fact that the PI3K Inhibitor LY294002 abolished the protective effects of QUE. Moreover, inhibition of Apoptosis, but not promotion of myogenesis, directly alleviated DON-induced muscle defects, establishing Apoptosis as the causative event. In conclusion, our data demonstrated that QUE alleviated DON-induced Apoptosis via the PI3K/Akt/mTOR pathway, thereby mitigating muscle development disorders.

Keywords

Apoptosis; Deoxynivalenol; Muscle development disorder; PI3K/Akt/mTOR pathway; Quercetin.

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