RESUMEN
Necrotising enterocolitis (NEC) is a serious intestinal disease that occurs in the neonatal period. The present study aimed to investigate the protective effect of vitamin D on NEC and the underlying mechanisms. Artificial feeding and hypoxiacold stimulation were used to establish a mouse NEC model. IEC6 cells were treated with lipopolysaccharide (LPS) to establish the in vitro NEC model. Changes in the levels of interleukin (IL)6, IL1ß and tumour necrosis factor (TNF)α, and activities of malondialdehyde (MDA) and glutathione peroxidase (GPx) were investigated via ELISA kits. In addition, mRNA expression of IL6, IL1ß and TNFα and protein expression of phosphorylated (p)ERK1/2, Ki67, cleaved caspase3 and Bcl2 in intestinal tissues were determined via reverse transcriptionquantitative PCR and western blotting. Cell proliferation and apoptosis were also analysed via MTT assay and flow cytometry. In NEC mice, vitamin D reduced intestinal tissue damage, decreased the mRNA expression of IL6, IL1ß and TNFα, and decreased the protein expression of cleaved caspase3 and MDA. Whereas, vitamin D increased the protein expression of Bcl2 and Ki67 and GPx, as well as the pERK1/2/ERK1/2 ratio, in NEC mice. Furthermore, vitamin D improved cell viability, increased the ratio of pERK1/2/ERK1/2, inhibited apoptosis, and decreased the mRNA expression of IL6, IL1ß and TNFα in LPStreated IEC6 cells. The dualspecificity mitogenactivated protein kinase kinase inhibitor PD98059 reversed the effects of vitamin D on the proliferation, apoptosis and inflammation of LPStreated IEC6 cells. Overall, vitamin D relieved NEC in mice. Vitamin D promoted proliferation, and inhibited apoptosis and inflammation of LPStreated IEC6 cells by activating the ERK signalling pathway.
