Phosphatidylcholine regulates NF-κB activation in attenuation of LPS-induced inflammation: evidence from in vitro study. Issue 1 (2nd January 2018)

• Record Type: Journal Article
• Authors: Chen, Meijuan; Pan, Hongying; Dai, Yining; Zhang, Jiajie; Tong, Yongxi; Huang, Yicheng; Wang, Mingshan; Huang, Haijun
• Is Part Of: Animal cells and systems. Volume 22:Issue 1(2018)
• Page Start: 7
• Page End: 14
• Publication Date: 2018-01-02
• Subjects: Phosphatidylcholine -- LPS-induced injury -- tTNF-ɑ secretion and activation -- p65 nuclear translocation -- MAPKs signal pathway; Systems biology -- Periodicals; Biology -- Periodicals; Cytology -- Periodicals; Zoology -- Periodicals; 590
• DOI: 10.1080/19768354.2017.1405072
• Languages: English
• ISSNs: 1976-8354

Abstract

ABSTRACT: Phosphatidylcholine (PC) has been demonstrated as anti-inflammatory and antioxidant/pro-oxidant molecules. In this study, we investigated the protective effects of PC on inflammatory bowel disease (IBD) caused by lipopolysaccharide (LPS)-induced injury in intestinal epithelia cells. The IEC-6 cells (intestinal epithelia cells) were stimulated with LPS (1 μg/mL) for 24 h with or without PC pretreatment, in the next steps: (1) the level of the inflammatory cytokine tumor necrosis factor (TNF)-α was measured with ELISA; (2) the nuclear translocation and phosphorylation of NF-κB was investigated with Western blot, EMSA, immunofluorence assay; (3) the protein phosporylation levels in MAPK signaling pathway were detected with Western blot method. The results showed: (1) compared with the normal group, 10 and 20 μg/mL of PC significantly inhibited the production and activation of TNF-α, ( P < 0.01); (2) pretreatment with PC inhibited LPS-induced nuclear translocation and phosphorylation of p65 in IEC-6 cells; (3) pretreatment with PC inhibited the protein phosphorylation levels in MAPK signaling pathway. Our findings indicated that PC had the effect to protect IEC-6 cells from LPS-induced injury and this effect was exerted possibly through inhibiting the TNF-ɑ secretion, down-regulating nuclear translocation and phosphorylation of p65 and inhibiting MAPK signaling pathways.