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Folly Beach Library
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Wando Mount Pleasant Library
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Village Library
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Human Milk Oligosaccharides Activate Epidermal Growth Factor Receptor and Protect Against Hypoxia-Induced Injuries in the Mouse Intestinal Epithelium and Caco2 Cells.
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- Author(s): Wang, Chenyuan (AUTHOR); Zhang, Ming (AUTHOR); Guo, Huiyuan (AUTHOR); Yan, Jingyu (AUTHOR); Chen, Lingli (AUTHOR); Teng, Wendi (AUTHOR); Ren, Fazheng (AUTHOR); Li, Yiran (AUTHOR); Wang, Xifan (AUTHOR); Luo, Jie (AUTHOR); Li, Yixuan (AUTHOR)
- Source:
Journal of Nutrition. Apr2020, Vol. 150 Issue 4, p756-762. 7p. - Source:
- Additional Information
- Subject Terms: BOARD of Governors of the Federal Reserve System (U.S.); EPIDERMAL growth factor receptors; OLIGOSACCHARIDES; BREAST milk; INTESTINAL injuries; HYPOXIA-inducible factor 1; NEONATAL necrotizing enterocolitis; ANIMAL populations; RESEARCH; ANIMAL experimentation; RESEARCH methodology; CELL receptors; APOPTOSIS; CELL physiology; EVALUATION research; MEDICAL cooperation; COMPARATIVE studies; TRANSFERASES; INTESTINAL mucosa; PHOSPHORYLATION; MICE
- Abstract:
Background: Hypoxia-induced intestinal barrier injuries lead to necrotizing enterocolitis (NEC). Although NEC in preterm neonates is preventable by human milk oligosaccharides (HMOs), the underlying mechanism remains unknown.Objective: To reveal the role and mechanism of HMOs in protecting against hypoxia-induced injuries in intestinal epithelium of neonatal mice and cultured Caco2 cells.Methods: NEC was induced by hypoxia and cold stress. Seventy C57BL/C pups (7-d-old) were divided into 5 groups and fed maternal breast milk (BM), formula alone (FF), or the formula added with HMOs at 5 (LHMO), 10 (MHMO), or 20 mg/mL (HHMO) for 3 d. Ileal hypoxia inducible factor 1α (HIF1α) and cleaved Caspase 3 were determined, along with staining for Ki-67 protein to labeled proliferative cells. In vitro, adherent Caco2 cells (undifferentiated, passage 14) were treated with HMOs, galacto-oligosaccharides, fructo-oligosaccharides, or mixed oligosaccharides at 10 mg/mL for 1 d exposed to 1% O2. Cell proliferation and apoptosis, along with phosphorylated epidermal growth factor receptor (P-EGFR) and 38KD MAPK (P-P38), were assayed in differentiated or undifferentiated Caco2 cells.Results: Compared with the FF-fed mice, those fed MHMO and HHMO had 52% lower (P < 0.05) NEC scores, 60-80% greater (P < 0.05) KI67-positive cell numbers, and 56-71% decreases (P < 0.05) in ileal HIF1α and cleaved Caspase 3 (56-71%). Compared with those untreated, the HMO-treated Caco2 cells displayed 60% greater (P < 0.05) proliferative activity and 19% lower (P < 0.05) apoptotic cells after the hypoxia exposure. The HMO treatment led to 58% or 10-fold increases (P < 0.05) of P-EGFR and 48-89% decreases (P < 0.05) of P-P38 in either differentiated or undifferentiated Caco2 cells compared with the controls.Conclusion: Supplementing HMOs at 10-20 mg/mL into the formula for neonatal mice or media for Caco2 cells conferred protection against the hypoxia-induced injuries. The protection in the Caco2 cells was associated with an activation of EGFR. [ABSTRACT FROM AUTHOR] - Abstract: Copyright of Journal of Nutrition is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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