Effects of Quercetagetin on Gut-Liver Axis Function and Cecal Microbial Diversity in Broilers via...

Oxidative stress is a major constraint on broiler health and productivity. Mitochondrial dysfunction and gut-liver axis disruption play pivotal roles in this process. The present study investigated whether dietary quercetagetin (QG) alleviated diquat (DQ)-induced oxidative stress in broiler chickens through modulation of PINK1/Parkin-mediated mitophagy and gut-liver axis homeostasis. A total of 144 1-day-old WOD168 broilers were randomly assigned to four treatments with six replicate cages of six birds per cage: control group (non-challenged, basal diet), DQ group (DQ-challenged, basal diet), D_QG group (DQ-challenged, basal diet with 20 mg/kg QG), and QG group (non-challenged, basal diet with 20 mg/kg QG). On day 35, the DQ and D_QG groups were intraperitoneally administered DQ (20 mg/kg body weight). Dietary QG significantly increased body weight and attenuated the loss in average daily gain induced by DQ, while reducing serum aspartate aminotransferase levels. DQ challenge impaired gut barrier function, as indicated by decreased villus height, villus height/crypt depth ratio, and mRNA expression of Claudin-1 and ZO-1 (P < 0.05), exacerbated hepatic lesions, and significantly altered cecal microbial diversity. QG supplementation significantly attenuated the drop in glutathione peroxidase activity and downregulated PINK1 and LC3-II in hepatic mitochondria. It also significantly increased complex I activity, mitochondrial DNA copy number, and adenosine triphosphate content, while decreasing DQ-induced reactive oxygen species. Collectively, these results indicate that dietary QG alleviates DQ-induced oxidative stress by preserving mitochondrial function, potentially modulating PINK1/Parkin-related mitophagy, enhancing intestinal barrier integrity, and modulating cecal microbial composition.