Arabinogalactan Alleviates Lipopolysaccharide-Induced Intestinal Epithelial Barrier Damage through Adenosine Monophosphate-Activated Protein Kinase/Silent Information Regulator 1/Nuclear Factor Kappa-B Signaling Pathways in Caco-2 Cells

被引:5
作者
Zheng, Jiachen [1 ]
Gong, Shaoying [1 ]
Han, Jianchun [1 ,2 ]
机构
[1] Northeast Agr Univ, Coll Food Sci, Harbin 150030, Peoples R China
[2] Northeast Agr Univ, Heilongjiang Green Food Sci Res Inst, Harbin 150030, Peoples R China
关键词
arabinogalactan; intestinal epithelial barrier; tight junction proteins; intracellular calcium; oxidative stress; inflammatory; AMPK/SIRT1/NF-kappa B signaling pathway; TIGHT JUNCTIONS; IPEC-J2; CELLS; INFLAMMATION; DISRUPTION; APOPTOSIS; CALCIUM; GROWTH; ROS;
D O I
10.3390/ijms242015337
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Intestinal epithelial barrier (IEB) damage is an important aspect in inflammatory bowel disease (IBD). The objective of this study was to explore the protective effects and mechanisms of arabinogalactan (AG) on lipopolysaccharide (LPS)-stimulated IEB dysfunction. The results show that AG (1, 2, and 5 mg/mL) mitigated 100 mu g/mL LPS-stimulated IEB dysfunction through increasing transepithelial electrical resistance (TEER), reducing fluorescein isothiocyanate (FITC)-dextran (4 kDa) flux, and up-regulating the protein and mRNA expression of tight junction (TJ) proteins (Claudin-1, Zonula occludens-1 (ZO-1) and Occludin). In addition, AG ameliorated LPS-stimulated IEB dysfunction by reducing interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and IL-1 beta levels, decreasing the reactive oxygen species (ROS) level, increasing superoxide dismutase (SOD) activity, increasing the glutathione (GSH) level, and decreasing the levels of malondialdehyde (MDA) and intracellular calcium ([Ca2+]i). Furthermore, 2 mg/mL AG up-regulated the expression of silent information regulator 1 (SIRT1), the phosphorylated adenosine monophosphate-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor gamma coactivator (PGC)-1 alpha and inhibited the phosphorylation of nuclear factor kappa-B (NF-kappa B) and the inhibitor of NF-kappa B alpha (I kappa B alpha). Therefore, AG could maintain IEB integrity by activating AMPK/SIRT1 and inhibiting the NF-kappa B signaling pathway. In conclusion, AG can regulate the AMPK/SIRT1/NF-kappa B signaling pathway to reduce inflammation and oxidative stress, thus alleviating LPS-stimulated IEB damage.
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页数:13
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