Potential role of endoplasmic reticulum stress is involved in the protection of fish oil on neonatal rats with necrotizing enterocolitis.

Neonatal necrotizing enterocolitis (NEC) is a serious gastrointestinal disease with high death rate in premature infants. Fish oil (FO) and its constituents have been shown to ameliorate intestinal inflammation and mucosal damage. However, the underlying mechanism of action is not known. In the present study, we divided Sprague-Dawley rats into three groups: control group, NEC model group, and FO pre-feeding+NEC model group. Briefly, one week before NEC modeling, in addition to being fed with milk, the FO pre-feeding+NEC modeling group was fed with FO, the NEC group was fed with saline, and the control group was only inserted a gastric-tube for 7 days. Subsequently, histological assay, Western blot, and ELISA were performed. Pretreatment with FO attenuated the NEC symptoms, alleviated intestinal pathological injury, and decreased the expressions of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Furthermore, pretreatment with FO reduced the expressions of endoplasmic reticulum stress (ERS) related proteins, caspase-12, and glucose-regulated protein 78 (GRP78). In addition, intestinal histopathological scores showed a significant positive correlation with intestinal expressions of IL-6, TNF-α, and caspase-12. Collectively, these results indicate that ERS pathway might be involved in the effect of FO in alleviating intestinal mucosal inflammation and injury in rats with NEC.