Dietary Sodium Butyrate Alleviates Thiram-Induced Tibial Dyschondroplasia in Broilers by Improving Redox Homeostasis and Upregulating the Nrf2/HO-1 Pathway

Oxidative stress-induced impairment of chondrocyte differentiation and bone homeostasis is pivotal in tibial dyschondroplasia (TD). Sodium butyrate has been shown to modulate gut microbiota, improve redox homeostasis, and support skeletal metabolism; however, whether it exerts protection against TD specifically through oxidative stress modulation remains unclear. A total of 210 one-day-old male Arbor Acres broilers were randomly allocated to three treatment groups, with seven replicate pens per group and 10 birds per pen. The birds were housed in a windowless, climate-controlled indoor poultry house with floor pens and rice-husk bedding. In a thiram-induced broiler TD model, dietary sodium butyrate (500 mg/kg) reshaped the gut microbiota by increasing beneficial genera (Ligilactobacillus, Lactobacillus, Blautia, and Mediterraneibacter), decreasing Escherichia-Shigella abundance, and elevating ileal butyrate concentration. These shifts co-occurred with mitigated oxidative damage, including reduced ROS and MDA in both serum and ileal mucosa, partial elevations in SOD and GSH-Px activities, upregulated Nrf2 and HO-1 expression in both the ileal mucosa and tibial growth plate, and improved mitochondrial function in the ileal mucosa, as indicated by restored mitochondrial membrane potential, reduced superoxide anion levels, and increased respiratory chain complex I activity. Concomitantly, sodium butyrate improved growth performance and skeletal phenotypes, attenuating growth plate lesions and restoring tibial morphology and mineralization. It also favorably modulated bone metabolism by elevating the OPG/RANKL ratio and upregulating COL2A1 expression. Correlation analyses linked microbial alterations to antioxidant status and skeletal parameters. Collectively, these findings suggest that sodium butyrate alleviates thiram-induced TD in association with gut microbiota remodeling, which is correlated with enhanced redox homeostasis and bone metabolism, supporting a potential gut–bone axis mechanism.