Naringenin counteracts LPS-induced inflammation and immune deficits in chicken thymus by alleviating mtROS/ferroptosis levels

• Published in: Poultry science Vol. 103; no. 11; p. 104179
• Main Authors: Yu, Fei, Shi, Xu, Li, Ke, Yin, Yilin, Xu, Shiwen
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 01.11.2024; Elsevier
• Subjects: IMMUNOLOGY, HEALTH AND DISEASE; inflammation and immune function; mtROS/ferroptosis; naringenin; naringenin; inflammation and immune function; mtROS/ferroptosis
• ISSN: 0032-5791; 1525-3171; 1525-3171
• DOI: 10.1016/j.psj.2024.104179

Naringenin is a flavonoid with significant anti-inflammatory and antioxidant properties. Mitochondrial dynamics, the mitochondrial respiratory chain, and mtROS are closely related to each other and regulate various biological processes. Ferroptosis is closely related to inflammatory responses and immune function in multiple tissues and organs. However, whether naringenin can alleviate LPS-induced inflammation and immune disorders in the chicken thymus via mtROS/ferroptosis has not been reported. Therefore, in this study, we constructed chicken thymus and MSB-1 cell models of LPS and naringenin based on screening for naringenin concentrations that have positive effects on inflammation and immune function to further investigate the anti-inflammatory, antiferroptosis, and maintenance of the immune function of naringenin. The results showed that 40 mg/kg naringenin alleviated LPS-induced tissue damage, elevated serum inflammatory factors, and decreased serum immune factors. The mechanism by which naringenin attenuates mtROS release by alleviating the imbalance of mitochondrial dynamics and the blockage of the respiratory chain. The effect of naringenin on alleviating LPS-induced lipid peroxidation, disruption of the GSH/GSSG system, iron overload, and GPx4 inactivation, thereby attenuating ferroptosis in thymus tissue, was inhibited by the addition of mtROS activators. In conclusion, naringenin alleviates LPS-induced ferroptosis in chicken thymus by attenuating mtROS release.