Lactobacillus rhamnosus MY-1 alleviates deoxynivalenol-induced oxidative stress, inflammation, and gut microbiota dysbiosis both in vivo and In vitro

Yukai Lin¹Ruibiao Wang¹Jie Yao²Hanqing Zhao¹Zuhua Yu²Bo Wen¹Yan Yan Jia²Chengshui Liao²Rongxian Guo²Lei Wang¹Xiaojing Xia¹Yanzhao Xu¹Ke Ding^1*

• ¹Henan Institute of Science and Technology, Xinxiang, China
• ²Henan University of Science and Technology, Luoyang, China

Deoxynivalenol (DON), a common mycotoxin that contaminates grains and feed, poses a serious threat to animal health by inducing intestinal dysfunction. Although several probiotic strains have been reported to mitigate DON toxicity, the multifaceted protective effects of Lactobacillus rhamnosus MY-1—a strain with a high DON degradation rate and established safety profile—require further systematic evaluation. This study aimed to comprehensively assess the ability of Lactobacillus rhamnosus MY-1 to alleviate DON-induced oxidative stress, inflammation, and gut microbiota dysbiosis in vitro and in vivo, and to elucidate its underlying mechanisms. Using IPEC-J2 cells and a BALB/c mouse model, we investigated the effects of MY-1 on oxidative stress, inflammatory responses, apoptosis, tight junction integrity, and gut microbiota composition. The results showed that the MY-1 supernatant significantly restored IPEC-J2 cell viability and ameliorated DON-induced ultrastructural damage. Furthermore, MY-1 effectively alleviated oxidative stress by reducing malondialdehyde (MDA) levels and enhancing the total antioxidant capacity (T-AOC), while also inhibiting the expression of pro-inflammatory cytokines (TNF-α, IL-1α) and promoting the expression of the anti-inflammatory cytokine IL-4. In mice, MY-1 alleviated This is a provisional file, not the final typeset article DON-induced growth inhibition and pathological damage in the duodenum, jejunum, and ileum, restored the expression of tight junction proteins (ZO-1, Occludin, Claudin-1), and regulated apoptosis-related genes (BAX, Caspase-3, BCL-2). Gut microbiota analysis revealed that MY-1 alleviated DON-induced dysbiosis, evidenced by the restoration of alpha diversity indices (Chao1, Simpson, and Shannon) and structural separation in beta diversity. This was accompanied by modulation of dominant genera such as Bacteroides and Dubosiella, which were elevated in the DON group. In summary, this systematic study demonstrates that Lactobacillus rhamnosus MY-1 exerts comprehensive protective effects against DON-induced intestinal toxicity through integrated mechanisms including direct detoxification, antioxidant and anti-inflammatory activities, and microbiota modulation. These findings underscore the value of MY-1 as a well-characterized probiotic candidate for mitigating mycotoxin effects in animal production.