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

## TL;DR

Lactobacillus rhamnosus MY-1 reduces the harmful effects of a mycotoxin on the gut by fighting oxidative stress, inflammation, and microbiota imbalance in both cells and mice.

## Contribution

Demonstrates the comprehensive protective effects of L. rhamnosus MY-1 against deoxynivalenol toxicity through multiple mechanisms.

## Key findings

- MY-1 reduces oxidative stress and inflammation in intestinal cells exposed to deoxynivalenol.
- MY-1 restores gut microbiota diversity and tight junction proteins in mice affected by deoxynivalenol.
- MY-1 modulates harmful and beneficial gut bacteria genera like Bacteroides and Dubosiella.

## Abstract

Deoxynivalenol (DON), a prevalent mycotoxin in grains and feed, poses a serious threat to animal health by inducing intestinal dysfunction. While some probiotics are known to mitigate DON toxicity, the multifaceted protective effects of Lactobacillus rhamnosus MY-1—a strain with high DON-degradation capacity and a proven safety profile—require comprehensive evaluation. This study aimed to systematically assess the ability of MY-1 to alleviate DON-induced oxidative stress, inflammation, and gut microbiota dysbiosis, and to elucidate its underlying mechanisms.

Investigations were conducted in vitro using IPEC-J2 cells and in vivo using a BALB/c mouse model. We examined the effects of MY-1 on cell viability, ultrastructure, oxidative stress markers (MDA, T-AOC), inflammatory cytokines (TNF-α, IL-1α, IL-4), apoptosis-related genes (BAX, Caspase-3, BCL-2), and tight junction protein (ZO-1, Occludin, Claudin-1) expression. Gut microbiota composition was analyzed via alpha (Chao1, Simpson, Shannon) and beta diversity indices.

The MY-1 supernatant restored IPEC-J2 cell viability and ameliorated DON-induced ultrastructural damage. MY-1 alleviated oxidative stress by reducing MDA and enhancing T-AOC, while inhibiting pro-inflammatory cytokines (TNF-α, IL-1α) and promoting the anti-inflammatory cytokine IL-4. In mice, MY-1 mitigated DON-induced growth inhibition and intestinal pathological damage, restored tight junction protein expression, and regulated apoptosis-related genes. Gut microbiota analysis showed that MY-1 reversed DON-induced dysbiosis, restoring alpha diversity and beta diversity structure, and modulated the abundances of dominant genera such as Bacteroides and Dubosiella.

This 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.