Peer-reviewed veterinary case report
How berberine protects dog corneal cells from bacterial damage
By Liang, Yuxuan et al.·Published in Experimental eye research·2026·College of Veterinary Medicine, China·View original on PubMed →
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Original publication title: Berberine inhibits muramyl dipeptide-induced oxidative stress and pyroptosis in canine corneal epithelial cells via the NOD2 signaling pathway.
- Species:
- dog
Plain-English summary
A study found that a natural compound called berberine can help treat bacterial keratitis, a serious eye infection in dogs that can lead to corneal ulcers and vision loss. When canine corneal cells were exposed to a bacterial component, it triggered inflammation and oxidative stress, worsening the condition. However, berberine effectively reduced this inflammation and oxidative damage by blocking the harmful signaling pathway involved. This suggests that berberine could be a promising treatment option for dogs suffering from this eye infection, potentially helping to protect their vision and overall eye health.
People also search for: dog eye infection treatment · berberine for dogs · bacterial keratitis in dogs · corneal ulcer in dogs
Abstract
Bacterial keratitis poses a significant threat to ocular health in companion animals, particularly dogs, often leading to corneal ulceration and visual impairment. Muramyl dipeptide (MDP), a conserved bacterial peptidoglycan motif, activates nucleotide-binding oligomerization domain-containing protein 2 (NOD2), yet its contribution to corneal pathogenesis remains incompletely defined. This study demonstrated that MDP induced the NOD2-dependent activation of the RIPK2/NF-κB pathway, triggering pro-inflammatory cytokine production and suppressing the Nrf2-mediated antioxidant response, thereby exacerbating oxidative stress in canine corneal epithelial cells. Furthermore, MDP promoted NLRP3 inflammasome assembly, caspase-1 activation, and gasdermin D-mediated pyroptosis. Inhibition of NOD2 signaling attenuated these effects, highlighting its central role in coordinating inflammatory and oxidative damage. Notably, the natural compound berberine (BBR) effectively suppressed NOD2 activation, restored redox homeostasis, and inhibited pyroptosis in both cellular and canine models of MDP-induced keratitis. These results revealed a previously unrecognized mechanism by which MDP exacerbated corneal damage through NOD2-driven integration of oxidative stress and pyroptosis. We also identified BBR as a multi-target therapeutic agent capable of disrupting this pathogenic cascade. Our findings provided mechanistic insights into the treatment of bacterial keratitis through modulation of innate immune signaling pathways.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/41724227/