Protective effects of lactoferrin on injured intestinal epithelial cells

Lactoferrin has been used as a milk supplement to prevent disease progression in necrotizing enterocolitis. However, the underlying mechanism is still unclear. We hypothesize that lactoferrin administration can modulate intestinal epithelial cell injury.

We established an in vitro model of epithelial cell injury by treating rat intestinal epithelial cells IEC-18 and human Caco-2 cells with hydrogen peroxide (H₂O₂), while lactoferrin was added as treatment at the same time. Live/dead cells were detected by immunofluorescence. Gene expression of inflammatory markers interleukin-6 (IL-6), intestinal stem cells (Lgr5), and proliferation marker (Wnt/β-catenin) were measured. Data was presented as mean ± SEM and compared using one-way ANOVA. A p-value <0.05 was considered significant.

Compared to control cells, H₂O₂ induced cell death in both IEC-18 and Caco-2 cells, whereas treatment with lactoferrin maintained cell viability. In addition, lactoferrin reduced gene expression of IL-6, while it increased gene expression of Lgr5 and Wnt/β-catenin.

Intestinal cell injury can be induced by exposure to H₂O₂, mimicking epithelial damage during intestinal injury. This damage can be reversed by lactoferrin administration by reducing inflammation and inducing cell proliferation. Lactoferrin can be a potential pharmacological intervention for the prevention and recovery of intestinal epithelial injury.