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Nauclea officinalis inhibits inflammation in LPS-mediated RAW 264.7 macrophages by suppressing the NF-κB signaling pathway.

Authors :
Zhai, Xiao-Ting
Zhang, Zhi-Yuan
Jiang, Cui-Hua
Chen, Jia-Quan
Ye, Ji-Qing
Jia, Xiao-Bin
Yang, Yi
Ni, Qian
Wang, Shu-Xia
Song, Jie
Zhu, Fen-Xia
Source :
Journal of Ethnopharmacology. May2016, Vol. 183, p159-165. 7p.
Publication Year :
2016

Abstract

Ethnopharmacological relevance Nauclea officinalis has been traditionally used in China for the treatment of fever, pneumonia and enteritidis etc. This study aims to investigate effects of N. officinalis on the inflammatory response as well as the possible molecular mechanism in LPS-stimulated RAW 264.7 murine macrophage cells. Materials and methods Anti-inflammatory activity of N. officinalis (10, 20, 50, and 100 µg/mL) was investigated by using LPS-induced RAW 264.7 macrophages. The NO production was determined by assaying nitrite in culture supernatants with the Griess reagent. The levels of TNF-α, IL-6 and IL-1β in culture media were measured with ELISA kits. Real time fluorescence quantitative PCR was detected for mRNA expression of iNOS, TNF-α, IL-6 and IL-1β. Western blot assay was performed to illustrate the inhibitory effects of N. officinalis on phosphorylation of IκB-α and NF-κB p65. Results Treatment with N. officinalis (10–100 µg/mL) dose-dependently inhibited the production as well as mRNA expression of NO, TNF-α, IL-6 and IL-1β in RAW 264.7 macrophages. Western blot assay suggested that the mechanism of the anti-inflammatory effect was associated with the inhibition of phosphorylation of IκB-α and NF-κB p65. Conclusions The results indicated that N. officinalis potentially inhibited the activation of upstream mediator NF-κB signaling pathway via suppressing phosphorylation of IκB-α and NF-κB p65 to inhibit LPS-stimulated inflammation. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
03788741
Volume :
183
Database :
Academic Search Index
Journal :
Journal of Ethnopharmacology
Publication Type :
Academic Journal
Accession number :
114023267
Full Text :
https://doi.org/10.1016/j.jep.2016.01.018