Reduced apoptosis in newborn compared to adult rat intestine after ischemia-reperfusion injury

Chih Cheng Luo, Hsiang Hung Shih, Cheng Hsun Chiu, Wei Chun Ma, Hui Ying Chung

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


The pathogenesis of necrotizing enterocolitis (NEC) is unknown. Ischemia and reperfusion (I/R) injury has been considered to be a major contributing factor. More recent reports have noted that apoptosis is a significant and perhaps the principal contributor to cell death after I/R. Some reports revealed that infants with NEC and perforated bowel can completely recover with drainage alone. This study aims to assess the ability of newborn rat intestine to resist apoptosis after I/R injury compared with adult rat intestine. Intestines from 10 groups of rats (n = 6 for each study group) were studied: (1) normal control group; (2) ischemia group, receiving vascular occlusion for 60 min; (3) I/R groups receiving vascular occlusion for 60 min and reperfusion for 15, 30, and 60 min, respectively. Apoptosis was quantified by TUNEL methods. Statistical analysis was performed using ANOVA with Dunn's test. TUNEL-positive cells per 10 crypts were significantly increased in the ischemia and I/R groups compared to the control group. The peak number of positive cells by TUNEL was recognized 30 min after reperfusion in adult and newborn rats and then reduced gradually. The newborn rats had significantly less TUNEL-positive cells per 10 crypts than adult rats subjected to I/R injury (p <0.05). We demonstrated that the activation of apoptosis occurred after intestinal I/R injury, especially during the reperfusion phase. The newborn intestine was more resistant to I/R injury and thus may have significant clinical application.

Original languageEnglish
Pages (from-to)90-93
Number of pages4
JournalBiology of the Neonate
Issue number2
Publication statusPublished - 2004
Externally publishedYes


  • Apoptosis
  • Ischemia-reperfusion injury
  • Small intestine

ASJC Scopus subject areas

  • Developmental Biology
  • Pediatrics, Perinatology, and Child Health


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