Evaluation of the protective and therapeutic effects of extra virgin olive oil rich in phenol in experimental model of neonatal necrotizing enterocolitis by clinical disease score, ınflammation, apoptosis, and oxidative stress markers
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In brief
In brief
This experimental study demonstrates that phenol-rich extra virgin olive oil significantly reduces intestinal damage in a neonatal rat model of necrotizing enterocolitis by suppressing inflammation, oxidative stress, and apoptosis. Treatment improved clinical outcomes, reduced inflammatory markers (IL-1β, IL-6), and decreased histopathological injury scores.
- Phenol-rich extra virgin olive oil significantly reduced clinical disease severity and improved weight gain in experimental neonatal NEC.
- EVOO treatment decreased pro-inflammatory cytokines (IL-1β, IL-6) and oxidative stress markers (MDA) in NEC-induced intestinal injury.
- EVOO reduced intestinal apoptosis (Caspase-3 positive cells) and histopathological damage scores in experimental NEC models.
- High-phenolic EVOO shows promise as both protective and therapeutic intervention for NEC through anti-inflammatory and antioxidant mechanisms.
Written by the GCMD Library team from the article.
Abstract
Background and aim
Necrotizing Enterocolitis (NEC) is an inflammation-associated ischemic necrosis of the intestine. To investigate the effects of extra virgin olive oil (EVOO) on inflammation, oxidative stress, apoptosis, and histological changes in NEC-induced newborn rats.
Materials and methods
24 rats were randomly divided into three groups: control, NEC and NEC + EVOO. NEC induction was performed using hypoxia–hyperoxia, formula feeding, and cold stress. The NEC + EVOO group received 2 ml/kg EVOO with high phenolic content by gavage twice a day for 3 days. 3 cm of bowel including terminal ileum, cecum, and proximal colon was excised.
Results
Weight gain and clinical disease scores were significantly higher in the NEC + EVOO group than in the NEC group (p < 0.001). EVOO treatment caused significant decreases in IL1β, IL6 levels (p = 0.016, p = 0.029 respectively) and EGF, MDA levels (p = 0.032, p = 0.013 respectively) compared to NEC group. Significant decreases were observed in IL6 gene expression in the NEC + EVOO group compared to the NEC group (p = 0.002). In the group NEC + EVOO, the number of Caspase-3 positive cells was found to be significantly reduced (p < 0.001) and histopathological examination revealed minimal changes and significantly lower histopathological scores (p < 0.001).
Conclusion
Phenol-rich EVOO prevents intestinal damage caused by NEC by inhibiting inflammation, oxidative stress, apoptosis.