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Updated: Jun 10, 2026
A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis
Published on: November 30, 2021
Serum vitamin A and E improve neonatal necrotizing enterocolitis through activation of SOD/GPx pathway
1Department of Clinical Nutrition, West China Hospital of Sichuan University, Chengdu, Sichuan, 610041, China.
Insights
Vitamins A and E may protect newborns from necrotizing enterocolitis (NEC). Supplementation reduced inflammation and intestinal damage by activating the SOD/GPx pathway, suggesting a key role in infant gut health.
Area of Science:
- Neonatal Medicine
- Nutritional Immunology
- Gastroenterology
Background:
- Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease affecting newborns.
- Vitamins A and E are recognized for their anti-inflammatory and immune-modulating properties.
Purpose of the Study:
- To elucidate the mechanisms by which vitamins A and E impact neonatal NEC.
- To investigate the role of these vitamins in modulating NF-κB, gut microbiota, and inflammatory cytokines.
Main Methods:
- Serum vitamin A and E levels were quantified in healthy and NEC neonates and mice.
- An experimental NEC model was utilized, with interventions including vitamin A/E supplementation, SOD/GPx inhibition (DDC), and SOD/GPx activation (DDW).
- Intestinal pathology and serum inflammatory markers were assessed post-intervention.
Main Results:
- NEC subjects exhibited significantly lower serum vitamin A and E levels, inversely correlated with disease severity.
- Vitamin A or E supplementation ameliorated intestinal damage in NEC mice.
- Combined vitamin A and E treatment synergistically activated the SOD/GPx pathway, enhancing anti-inflammatory effects and improving NEC symptoms.
Conclusions:
- Vitamins A and E show potential in mitigating NEC by modulating inflammatory responses through the SOD/GPx pathway.
- The observed correlation between vitamin levels and NEC severity highlights their importance in maintaining intestinal homeostasis.
- Further research into the microbiota-modulating effects of vitamins A and E in NEC is warranted.
Background:
Colitis, including necrotizing enterocolitis (NEC), is a common and serious disease in newborns.
Objectives:
This study aimed to investigate the specific mechanisms of vitamins A and E in neonatal NEC, given their known roles in inhibiting NF-κB, regulating intestinal flora and reducing inflammatory cytokines.
Methods:
The study measured serum vitamin A and E levels in healthy and NEC newborns/mice. An NEC model was established and mice were treated with vitamins A/E, DDC (SOD/GPx inhibitor), or DDW (SOD/GPx activator). Serum vitamin levels and intestinal inflammatory factors were then assessed.
Results:
NEC subjects showed significantly lower vitamin A and E levels, which correlated negatively with disease severity. NEC mice exhibited intestinal pathological damage. Vitamin A or E supplementation alleviated this damage and their combination synergistically activated the SOD/GPx pathway, enhancing anti-inflammatory effects. Further inhibition of inflammation and improvement in symptoms were achieved using the SOD/GPx activator DDW.
Conclusion:
Vitamins A and E may alleviate NEC potentially by modulating inflammatory responses via the SOD/GPx pathway. The correlation between vitamin levels and disease severity suggests a role in intestinal homeostasis, warranting further investigation into microbiota modulation.
