Lactiplantibacillus plantarum JM113 alleviates mitochondrial dysfunction induced by deoxynivalenol in the jejunum of broiler chickens

Mitochondria are primary targets of deoxynivalenol (DON), which play a pivotal role in maintaining intestinal health. It has been suggested that Lactiplantibacillus plantarum JM113 (L. plantarum JM113) exhibits protective effects against the enterotoxicity of DON in broilers. However, the changes in mitochondrial homeostasis during this process remain unclear. A total of 144 one-day-old Arbor Acres broilers were randomly assigned to 3 groups, including the CON group (fed a basal diet and gavaged with 0.5 mL PBS), the DON group (supplemented with 5 mg/kg DON based on the CON group) and the DJ group (fed a basal diet challenged with 5 mg/kg DON and gavaged with 1 × 10⁹ CFU L. plantarum JM113). The results showed that deoxynivalenol damaged mitochondrial morphology in the jejunum, characterized by swelling, vacuolation and cristae disruption, while L. plantarum JM113 reversed these alterations. Furthermore, the DON treatment significantly decreased total antioxidant capacity (T-AOC) in the jejunum compared with the CON group at both 7-day-old and 21-day-old, and T-AOC of the jejunum and jejunal mitochondria in the DJ group were notably increased at 21-day-old (P < 0.05). Compared to the DON group, the DJ group showed significantly upregulated expression of Mfn1, Mfn2, and Opa1 involved in mitochondrial fusion, and significantly downregulated expression of Drp1 and Fis1 mediated mitochondrial fission at 21-day-old (P < 0.05). Dietary DON exposure also induced inhibition of genes linked to mitochondrial biogenesis at 21-day-old, such as NRF1, NRF2, TFAM and PGC-1α, while L. plantarum JM113 reversed this state (P < 0.05). Additionally, oral administration of L. plantarum JM113 significantly inhibited the overactivation of mitophagy related genes and proteins in the jejunum caused by DON (P < 0.05). Moreover, L. plantarum JM113 alleviated jejunal apoptosis in broilers exposed to DON, manifested by a significant decrease in mRNA and protein expression of Bax and CASP3 (P < 0.05). In summary, L. plantarum JM113 alleviated oxidative stress induced by DON, improved mitochondrial homeostasis, and ultimately prevented the occurrence of apoptosis.