ArticlePediatric surgery international2011
Protective effects of caffeic acid phenethyl ester (CAPE) on intestinal damage in necrotizing enterocolitis.
Article in Pediatric surgery international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Food Additives, a Key Environmental Factor in the Development of IBD through Gut Dysbiosis.Microorganisms · 2022Review
- Mechanism of Neonatal Intestinal Injury Induced by Hyperoxia Therapy.Journal of immunology research · 2022Review
- AFB1 Induced Transcriptional Regulation Related to Apoptosis and Lipid Metabolism in Liver of Chicken.Toxins · 2020Article
- The mitochondrial and endoplasmic reticulum pathways involved in the apoptosis of bursa of Fabricius cells in broilers exposed to dietary aflatoxin B1.Oncotarget · 2016Article
- The mitochondrial and death receptor pathways involved in the thymocytes apoptosis induced by aflatoxin B1.Oncotarget · 2016Article
- Ameliorating effects of CAPE on oxidative damage caused by pneumoperitoneum in rat lung tissue.International journal of clinical and experimental medicine · 2014Article
- GLP-2 delays but does not prevent the onset of necrotizing enterocolitis in preterm pigs.Journal of pediatric gastroenterology and nutrition · 2013Article
- Caffeic acid phenethyl ester protects 661W cells from H2O2-mediated cell death and enhances electroretinography response in dim-reared albino rats.Molecular vision · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo determine the preventative effect of caffeic acid phenethyl ester (CAPE) in necrotizing enterocolitis (NEC) in an experimental rat model of NEC. MATERIALS AND
methodsThirty newborn Sprague-Dawley rats were randomly divided into three groups; as NEC, NEC + CAPE and control. NEC was induced by enteral formula feeding, subjected to hypoxia-hyperoxia and cold stress. Pups in the NEC + CAPE group were treated with CAPE at a dose of 30 mg/kg daily by intraperitoneal route from the first day to the end of the study. All pups were executed on the fourth day. Proximal colon and ileum were allocated for histopathologic and biochemical evaluation, including xanthine oxidase (XO), total antioxidant status (TAS), total oxidant status (TOS), malonaldehyde (MDA) and myeloperoxidase (MPO) activities.
resultsThe pups in the NEC + CAPE group had better histopathologic and apoptosis evaluations (TUNEL and caspase-9) and the severity of bowel damage was significantly lower in the NEC + CAPE group compared to the NEC group (P < 0.01). The clinical sickness scores and body weight in the NEC + CAPE group was significantly better compared to the NEC group (P < 0.05). Tissue MDA, MPO, XO levels and TOS were remarkably reduced in the NEC + CAPE group, however, TAS was significantly increased in the NEC + CAPE group (P < 0.05).
conclusionTreatment with CAPE reduces the intestinal damage in NEC.
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