Objective: Necrotizing enterocolitis (NEC) is a serious neonatal disease; this study aims to investigate the role of sulforaphane (SFN) in NEC-induced intestinal injury.

Methods: An animal model of NEC was established in newborn mice and intragastrically administrated with SFN; then, the general status and survival of the mice were observed. H&E staining was used to observe the pathological changes of intestinal tissues. ELISA, immunohistochemical staining, and flow cytometry assays were used to detect the levels of inflammatory factors, including TNF-, IL-6, and IL-17, the expression of Bax, Bcl-2, TLR4, and NF-B, and the percentages of the Th17 and Treg cells, respectively. GSK-3 expression levels were measured by immunofluorescence. IEC-6 and FHC cells were induced with LPS to mimic NEC in vitro and coincubated with SFN; then, the inflammatory factor levels and cell apoptosis rate were detected. Finally, Western blot was used to assess the expression of PI3K/Akt/GSK-3 pathway-related proteins in vitro and in vivo.

Results: SFN improved the survival rate of NEC mice during modeling, alleviated the severity of the intestinal injury, and reduced the proportion of Th17/Treg cells. SFN could inhibit TLR4 and NF-B levels, decrease the release of inflammatory factors TNF- and IL-6, suppress Bax expression, increase Bcl-2 expression, and inhibit apoptosis both in in vitro and in vivo models of NEC. Meanwhile, SFN regulated the expression of PI3K/Akt/GSK-3 pathway-related proteins in vitro and in vivo.

Conclusion: SFN relieved the inflammatory response and apoptosis by regulating the PI3K/Akt/GSK-3 signaling pathway, thereby alleviating NEC in model mice and cells.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9117068PMC
http://dx.doi.org/10.1155/2022/6529842DOI Listing

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