Pediatric research · 2026
Protective effects of enteral acetate supplementation against brain injury in a rat model of necrotizing enterocolitis.
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Hou Qiang, Ji Hong
Аннотация
BACKGROUND: Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease in preterm infants, often leading to brain injury. The microbiota-gut-brain axis (MGBA) plays a key role, with short-chain fatty acids (SCFAs) emerging as potential therapeutic agents. This study explores the impact of SCFAs, particularly acetate, in mitigating NEC-related brain injury.
METHODS: A NEC rat model was established via overfeeding, hypoxia, and asphyxia. Intestinal injury, SCFA levels, systemic inflammation, and neuroinflammation were assessed through histology, gas chromatography-mass spectrometry, ELISA, and Western blotting. Cognitive function was evaluated using the Morris water maze test.
RESULTS: NEC rats exhibited significantly lower levels of intestinal SCFAs, particularly acetate, compared to control rats. These reductions were accompanied by systemic inflammation, neuroinflammation and cognitive deficits. Supplementation with sodium acetate mitigated both intestinal and neuroinflammatory responses and improved cognitive function.
CONCLUSIONS: Acetate depletion contributes to NEC-associated brain injury, and early acetate supplementation may offer a promising therapeutic strategy to mitigate intestinal damage, neuroinflammation, and cognitive impairment.
IMPACT: Identifies acetate depletion as a key factor in NEC-related brain injury. Demonstrates that sodium acetate supplementation mitigates neuroinflammation and cognitive impairment. Expands understanding of the microbiota-gut-brain axis in NEC pathophysiology. Highlights SCFAs as potential therapeutic agents for NEC-related complications. Suggests a novel intervention strategy to improve neurodevelopmental outcomes in preterm infants.
METHODS: A NEC rat model was established via overfeeding, hypoxia, and asphyxia. Intestinal injury, SCFA levels, systemic inflammation, and neuroinflammation were assessed through histology, gas chromatography-mass spectrometry, ELISA, and Western blotting. Cognitive function was evaluated using the Morris water maze test.
RESULTS: NEC rats exhibited significantly lower levels of intestinal SCFAs, particularly acetate, compared to control rats. These reductions were accompanied by systemic inflammation, neuroinflammation and cognitive deficits. Supplementation with sodium acetate mitigated both intestinal and neuroinflammatory responses and improved cognitive function.
CONCLUSIONS: Acetate depletion contributes to NEC-associated brain injury, and early acetate supplementation may offer a promising therapeutic strategy to mitigate intestinal damage, neuroinflammation, and cognitive impairment.
IMPACT: Identifies acetate depletion as a key factor in NEC-related brain injury. Demonstrates that sodium acetate supplementation mitigates neuroinflammation and cognitive impairment. Expands understanding of the microbiota-gut-brain axis in NEC pathophysiology. Highlights SCFAs as potential therapeutic agents for NEC-related complications. Suggests a novel intervention strategy to improve neurodevelopmental outcomes in preterm infants.