Naringenin ameliorate heat stress induced hearts injury by regulating ferroptosis and ferritinophagy in chicken

Intensive farming and global warming exacerbate the impact of heat stress 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 heat stress-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 heat stress 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, heat stress 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 heat stress levels and alleviates heat-stress-induced damage to chicken hearts. Thus, it offers a new way to explore the prevention of heat stress in chickens.