Vitamin D3 mitigates lipopolysaccharide-induced oxidative stress, tight junction damage and intestinal inflammatory response in yellow catfish, Pelteobagrus fulvidraco

The present study explored the possible mitigative effects of vitamin D-3 (VD3) on lipopolysaccharide (LPS)-induced intestinal oxidative stress, inflammatory response and tight junction damage in yellow catfish, Pelteobagrus fulvidraco. Herein, four experimental groups were established by injecting yellow catfish with NaCl, LPS, VD3 or LPS plus VD3. The results showed that LPS induced oxidative stress and that exogenous VD3 mitigated the adverse effects of LPS. Additionally, LPS suppressed the activity of antioxidant enzymes (Cat, Sod and Gr) and upregulated the mRNA expression of proinflammatory cytokines (Tnf-alpha, Il-1 beta, Il-8). Furthermore, the mRNA expression of fencing tight junctions (Claudin-1, Claudin-5, Occludin, Zo-1) was downregulated, while that of pore-forming tight junctions (Claudin-2, Claudin-12) was upregulated, however no effect on apoptosis genes was observed (p53, Bax, Caspase-3 and Caspase-9). These LPS-induced effects were significantly reversed by pretreatment with VD3. Taken together, this study suggests that exogenous VD3 substantially alleviates LPS-induced intestinal inflammation by upregulating antioxidant activity, suppressing inflammation and promoting fencing tight junctions in the intestine.

Automated summary

The study revealed that exogenous VD3 substantially alleviates LPS-induced intestinal inflammation by upregulating antioxidant activity, suppressing inflammation, and promoting the expression of fencing tight junction genes in the intestine, while having no effect on apoptosis genes.