|Exosome type||Exosome origin||Exosome isolation||Exosome concentration||Exosome administration||Model||Modeling methoda||Main findings||Mechanism||Reference|
|AF-MSC-Ex||Rat||ExoQuick reagent||/||Intraperitoneal injection||
|Mouse pup with formula, exposure to hypoxia for 4 days and oral LPS injection (4 mg/kg for 2 days)||
AF-MSC-Exs increase cellular proliferation, reduce inflammation, and regenerate a normal epithelium.|
AF-MSC-Exs attenuate NEC intestinal injury via activating the Wnt signaling pathway.
Serial centrifugation (in vitro)|
PureExo Exosome Isolation kit (in vivo)
|~ 2.5 ×109 exosomes/50 μL||Intraperitoneal injection||
|Mouse pup with formula, hypoxia (100% N2, 1.5 min, bid for 4 days) and hypothermia (4 °C, 10 min, bid for 4 days)||
BM-MSC-Exs increase wound healing in vitro.|
BM-MSC-Exs significantly lower gut permeability and the incidence of NEC in vivo.
|AF-MSC-Ex||Rat||Ultra-centrifugation||4 × 108 exosomes/50 μL||Intraperitoneal injection||In vivo||Rat pups with formula, hypoxia (100% N2, 1.5 min, tid for 4 days) and hypothermia (4 °C, 10 min, tid for 4 days)||
BM-MSC-Exs, AF-MSC-Exs, amniotic fluid-derived NSC-Exs and enteric NSC-Exs demonstrate equivalent reductions in NEC incidence.|
Stem cell-derived exosomes are equivalent to stem cells in NEC therapy.
|NSC-Ex (amniotic fluid-derived)|
|HM-Ex||Human||Ultra-centrifugation||0–10 μg||/||In vitro||/||HM-Exs reduce oxidative stress-related injury on intestinal epithelial cells.||/|||
|HM-Ex||Human||Serial centrifugation||0.1 μg/μL||/||Ex vivo||/||
HM-Exs derived from colostrum, transitional or mature human milk prevent inflammatory injury.|
HM-Exs derived from colostrum are most effective in decreasing inflammatory cytokine.
|HM-Ex||Human||Ultra-centrifugation||200 μg/mL||Gavage||In vivo||Rat pups with formula and hypoxia (5% O2, 75% N2, 5 min, bid for 4 days)||
HM-Exs promote the proliferation and migration of intestinal epithelial cells both in vitro and in vivo.|
Peptidomic differences between preterm and term milk exosomes are revealed.
|HM-Ex||Human||Ultra-centrifugation||0–1 × 108 exosomes/100 μL||
|Rat pups with formula, hypoxia (< 1.5% O2, 1.5 min, tid for 4 days), hypothermia (4 °C, 10 min, tid for 4 days) and LPS (2 mg/kg, day 1)||
HM-Exs increase the proliferation and decrease the apoptosis of intestinal epithelial cells.|
HM-Exs administered intraperitoneally or enterally decrease NEC incidence.
HM-Ex enteral administration has better effects.
|Mouse pups with formula, hypoxia (5% O2, 10 min, tid for 5 days) and LPS (4 mg/kg, qd for 5 days)||
HM-Exs reduce inflammation and improve mucus production in vivo.|
HM-Exs decrease inflammation in hypoxia and LPS-treated intestinal organoids.
Pasteurized HM-Exs are as effective as raw HM-Exs.
|HM-Ex||Human||ExoQuick reagent||0.5 mg/mL||/||In vitro||/||HM-Exs upregulate Wnt/β-catenin signaling in ISCs and increase cell viability under H2O2 exposure compared to the control group.||Wnt/β-catenin (ISCs)|||
|Mouse pups with LPS (7.5 mg/kg, qd for 7 days)||
PM-Exs inhibit intestinal epithelial cell apoptosis and decrease TLR4/NF-κB signaling through miRNAs in vitro.|
PM-Exs prevent LPS-induced intestinal injury and inflammation in vivo.
|miRNAs (miR-4334, -219, -338)|||
|Mouse pups with formula, hypoxia (5% O2, 10 min, tid for 5 days) and LPS (4 mg/kg, day 6 and 7)||BovM-Exs promote goblet cell and endoplasmic reticulum chaperone protein expression both in vitro and in vivo, which increases mucus production and protect the intestine.||TFF3, MUC2 (goblet cell), and GRP94 (endoplasmic reticulum)|||