Effects of Quercetagetin on Gut-Liver Axis Function and Cecal Microbial Diversity in Broilers via PINK1/Parkin-Mediated Mitophagy

Oxidative stress is a major constraint on broiler health and productivity.Mitochondrial dysfunction and gut–liver axis disruption play pivotal roles in thisprocess. The present study investigated whether dietary quercetagetin (QG) alleviateddiquat (DQ)-induced oxidative stress in broiler chickens through modulation ofPINK1/Parkin-mediated mitophagy and gut–liver axis homeostasis. A total of 144 1-day-oldWOD168 broilers were randomly assigned to four treatments with six replicate cages ofsix 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 wereintraperitoneally administered DQ (20 mg/kg body weight). Dietary QG significantlyincreased body weight and attenuated the loss in average daily gain induced by DQ, whilereducing serum aspartate aminotransferase levels. DQ challenge impaired gut barrierfunction, as indicated by decreased villus height, villus height/crypt depth ratio, andmRNA expression of Claudin-1 and ZO-1 ( P < 0.05), exacerbated hepatic lesions, and significantly altered cecalmicrobial diversity. QG supplementation significantly attenuated the drop in glutathioneperoxidase 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 decreasingDQ-induced reactive oxygen species. Collectively, these results indicate that dietary QGalleviates DQ-induced oxidative stress by preserving mitochondrial function, potentiallymodulating PINK1/Parkin-related mitophagy, enhancing intestinal barrier integrity, andmodulating cecal microbial composition.