4.7 Article

Prevention of Necrotizing Enterocolitis through Milk Polar Lipids Reducing Intestinal Epithelial Apoptosis

期刊

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
卷 68, 期 26, 页码 7014-7023

出版社

AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.0c02629

关键词

neonatal necrotizing enterocolitis; milk polar lipids; cytokines; NF-kappa B pathway; apoptosis

资金

  1. National Natural Science Foundation of China [31972093, 31571852]
  2. Ningbo University State Key Laboratory for Quality and Safety of Agro-products [KF20190103]
  3. Jiangsu Agricultural Science and Technology Innovation Fund [CX (18) 3036]
  4. Jiangsu Science and Technology Department [BE 2018397]

向作者/读者索取更多资源

Neonatal necrotizing enterocolitis (NEC) is a common and devastating disease. The objective of this research was to investigate the protective mechanisms of milk polar lipids (MPLs) on the attenuation of lipopolysaccharides (LPS)-induced intestinal inflammation and apoptosis. MPLs were extracted from buttermilk and analyzed using ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). A neonatal NEC rat model was used to investigate the effects of MPLs on NEC and its underlying mechanisms. Hematoxylin-eosin (H&E) staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) assay were used to observe intestinal morphological changes and intestinal epithelial cell apoptosis, which showed that MPLs could reduce NEC symptoms and intestinal apoptosis. The expressions of IL-6, IL-8, and TNF-alpha in the MPL group was significantly downregulated (P < 0.05), and the expression levels of IL-10 were significantly upregulated (P < 0.05). At the same time, MPLs also significantly reduced (P < 0.05) activation of the LPS-induced TLR4/NF-kappa B signaling pathway. Furthermore, MPLs inhibit apoptosis by reducing the expressions of Bax, caspase-9, and caspase-3 and by increasing the expression of Bcl-2. In conclusion, MPLs could reduce NEC symptoms in mice by inhibiting cell inflammation and protecting against intestinal apoptosis.

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