Calenduloside E inhibits lipopolysaccharide-induced inflammatory response by inhibiting activation of ROS-mediated JAK1-stat3 signaling pathway in RAW264.7 cells.
10.12122/j.issn.1673-4254.2019.08.05
- Author:
Tuo TANG
1
;
Shengnan WANG
1
;
Tianyu CAI
2
;
Zhenyu CHENG
2
;
Shimei QI
1
;
Zhilin QI
1
Author Information
1. Department of Biochemistry and Molecular Biology, Wannan Medical College, Wuhu 241002, China.
2. Anhui Provincial Key Laboratory of Active Biological Macro-molecules, Wannan Medical College, Wuhu 241002, China.
- Publication Type:Journal Article
- Keywords:
JAK1-stat3 signaling pathway;
RAW264.7 cells;
calenduloside E;
inflammation;
lipopolysaccharide
- MeSH:
Animals;
Lipopolysaccharides;
Mice;
NF-kappa B;
Oleanolic Acid;
analogs & derivatives;
RAW 264.7 Cells;
Reactive Oxygen Species;
Saponins;
Signal Transduction
- From:
Journal of Southern Medical University
2019;39(8):904-910
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of calenduloside E on lipopolysaccharide (LPS)-induced inflammatory response in RAW264.7 cells and explore the underlying molecular mechanism.
METHODS:CCK-8 assay was used to examine the effect of different concentrations of calenduloside E (0-30 μg/mL) on the viability of RAW264.7 cells. The release of the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in RAW264.7 cells in response to pretreatment with 6, 8, and 10 μg/mL calenduloside E for 2 h followed by stimulation with 100 ng/mL LPS was detected using enzyme-linked immunosorbent assay (ELISA). The expression levels of iNOS and COX-2 and the activation of JAK-stats, MAPKs and NF-кB signaling pathways in the treated cells were determined using Western blotting. A reactive oxygen species (ROS) detection kit was used to detect ROS production in the cells, and the nuclear translocation of the transcription factor stat3 was observed by laser confocal microscopy.
RESULTS:Calenduloside E below 20 μg/mL did not significantly affect the viability of RAW264.7 cells. Calenduloside E dose-dependently decreased the expression levels of iNOS and COX-2 induced by LPS, inhibited LPS-induced release of TNF-α and IL-1β, and suppressed LPS-induced JAK1-stat3 signaling pathway activation and stat3 nuclear translocation. Calenduloside E also significantly reduced ROS production induced by LPS in RAW264.7 cells.
CONCLUSIONS:Calenduloside E inhibits LPS-induced inflammatory response by blocking ROS-mediated activation of JAK1-stat3 signaling pathway in RAW264.7 cells.
