Naringenin ameliorates heat-stress-induced heart injury by regulating ferroptosis and ferritinophagy in chickens.

Intensive farming and global warming exacerbate the impact of heat stress (HS) on the broiler industry, often causing significant heart damage to poultry and thus reducing production performance. Naringenin has garnered significant attention due to its potent antioxidant properties and cardioprotective characteristics. This article aims to explore the role of ferroptosis and ferritinophagy in HS-induced heart injury and evaluate the preventive effect of naringenin. The chickens were randomly allocated to four groups for the experiment. The experimental results indicate that HS can disrupt the homeostasis of heart antioxidant function and lead to the accumulation of free radicals in chickens. The accumulated reactive oxygen species result in heart damage. Moreover, HS upregulates the gene transcription and protein expression levels of ferroptosis-related indicators (GPX4, NRF2, ACSL4, TFR1) and ferritinophagy-related indicators (NCOA4, FTH1, P62, LC3B, BECN1). Meanwhile, naringenin intervention can effectively enhance heart antioxidant function and inhibit ferroptosis and ferritinophagy. It significantly reduces HS levels and alleviates heat-stress-induced damage to chicken hearts. Thus, it offers a new way to explore the prevention of HS in chickens.