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Prevention of Necrotizing Enterocolitis through Milk Polar Lipids Reducing Intestinal Epithelial Apoptosis.
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2020-06-09 , DOI: 10.1021/acs.jafc.0c02629
Yujie Yang 1 , Tao Zhang 1 , Guangyu Zhou 1 , Xiaoxiao Jiang 1 , Mingxuan Tao 1 , Jiaxin Zhang 1 , Xiaoqun Zeng 2 , Zhen Wu 2 , Daodong Pan 2 , Yuxing Guo 1
Affiliation  

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-α 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-κB 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.

中文翻译:

通过减少牛奶极性脂质减少肠道上皮细胞凋亡来预防坏死性小肠结肠炎。

新生儿坏死性小肠结肠炎(NEC)是一种常见的破坏性疾病。本研究的目的是研究乳极性脂质(MPL)对脂多糖(LPS)诱导的肠道炎症和细胞凋亡的缓解作用的保护机制。从酪乳中提取MPL,并使用超高效液相色谱-串联质谱(UPLC-MS / MS)进行分析。新生儿NEC大鼠模型用于研究MPL对NEC及其基础机制的影响。使用苏木精-伊红(H&E)染色和末端脱氧核苷酸转移酶介导的dUTP-生物素缺口末端标记(TUNEL)检测来观察肠道形态变化和肠道上皮细胞凋亡,这表明MPL可以减轻NEC症状和肠道凋亡。IL-6,IL-8,P <0.05),IL-10的表达水平显着上调(P <0.05)。同时,MPLs还显着降低(P <0.05)LPS诱导的TLR4 /NF-κB信号通路的激活。此外,MPL通过降低Bax,caspase-9和caspase-3的表达以及增加Bcl-2的表达来抑制细胞凋亡。总之,MPLs可以通过抑制细胞炎症和防止肠道凋亡来减轻小鼠的NEC症状。
更新日期:2020-07-01
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