# An organoid-based evaluation of Bacillus amyloliquefaciens SC06 in alleviating oxidative damage via Wnt signaling

**Authors:** Li Tang, Hao Wang, Qi Wang, Yang Wang, Xiang Li, Fei Wang, Qian Jin, Zihan Zeng, Aikun Fu, Xiaoliang Li, Weifen Li

PMC · DOI: 10.1186/s12917-026-05358-2 · BMC Veterinary Research · 2026-02-19

## TL;DR

This study shows how a probiotic, Bacillus amyloliquefaciens SC06, protects gut cells from oxidative damage by activating the Wnt signaling pathway.

## Contribution

The study identifies a novel probiotic-Wnt signaling mechanism that protects against oxidative stress in intestinal organoids.

## Key findings

- BaSC06 reduces oxidative stress and apoptosis in intestinal cells.
- BaSC06 promotes Paneth cell differentiation and activates the Wnt signaling pathway.
- Wnt pathway activation is essential for BaSC06's protective effects.

## Abstract

Bacillus amyloliquefaciens SC06 (BaSC06) has emerged as a promising probiotic for improving animal gut health and immuno-protection. However, the underlying molecular mechanisms remain incompletely understood. In this study, we employed porcine intestinal organoids as an ex vivo model and induced oxidative stress using diquat to systematically evaluate the protective effects of BaSC06. We evaluated antioxidant capacity, apoptosis-related markers, intestinal stem cells differentiation markers, and associated signaling pathways. Pretreatment with BaSC06 significantly alleviated oxidative damage by reducing intracellular reactive oxygen species levels and resultant apoptosis. Cellularly, BaSC06 promoted intestinal stem cells proliferation and favored differentiation toward Paneth cells while suppressing differentiation into other epithelial lineages. Mechanistically, these effects were mediated by the activation of the Wnt signaling pathway, and it was further confirmed by using a specific Wnt inhibitor. Overall, our findings uncover a probiotic-Wnt axis through which BaSC06 confers protection against oxidative stress, involving modulation of intestinal stem cells fate and enhancement of epithelial barrier function.

The online version contains supplementary material available at 10.1186/s12917-026-05358-2.

## Linked entities

- **Chemicals:** diquat (PubChem CID 6795)

## Full-text entities

- **Diseases:** PIO (MESH:D007410), ISCs (MESH:C567703), injury (MESH:D014947), cytotoxicity (MESH:D064420), inflammatory (MESH:D007249), mucosal injury (MESH:D052016), Necrotic (MESH:D009336)
- **Chemicals:** MDA (MESH:D008315), superoxide anions (MESH:D013481), DQ (MESH:D004178), PVDF (MESH:C024865), Ba (-), EDTA (MESH:D004492), ICG-001 (MESH:C492448), lipid (MESH:D008055), PI (MESH:D011419), SDS (MESH:D012967), PBS (MESH:D007854), 2',7'-dichlorofluorescin diacetate (MESH:C029569), ROS (MESH:D017382), ICG (MESH:D007208), DPBS (MESH:C012939)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Lactobacillus (genus) [taxon 1578]
- **Cell lines:** BaSC06 — Homo sapiens (Human), Melanoma, Cancer cell line (CVCL_S857)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13020122/full.md

## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC13020122/full.md

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Source: https://tomesphere.com/paper/PMC13020122