Fermented ginseng attenuates lipopolysaccharide-induced inflammatory responses by activating the TLR4/MAPK signaling pathway and remediating gut barrier

2021 ◽  
Author(s):  
Jingjing Fan ◽  
Sitong Liu ◽  
Zhiyi Ai ◽  
Yiying Chen ◽  
Yonghong Wang ◽  
...  

Generally, ginsenosides have the physiological effect of an anti-inflammatory immunity.

MedChemComm ◽  
2017 ◽  
Vol 8 (7) ◽  
pp. 1498-1504 ◽  
Author(s):  
Bo Li ◽  
Yongan Yang ◽  
Liuzeng Chen ◽  
Shichao Chen ◽  
Jing Zhang ◽  
...  

18α-GAMG exhibited strong anti-inflammatory activity through inhibiting the expression of iNOS, COX-2, and MAPKs, as well as activation of NF-κB.


2018 ◽  
Vol 6 (8) ◽  
pp. 2560-2567 ◽  
Author(s):  
Myung-hee Lee ◽  
Tae Gyu Nam ◽  
Inil Lee ◽  
Eun Ju Shin ◽  
Ah-ram Han ◽  
...  

2018 ◽  
Vol 51 (6) ◽  
pp. 2591-2603 ◽  
Author(s):  
Li Zang ◽  
Quan Hong ◽  
Guoqing Yang ◽  
Weijun Gu ◽  
Anping Wang ◽  
...  

Background/Aims: Chronic inflammation contributes to the development of type 2 diabetes mellitus by targeting the insulin receptor substrate protein-1 (IRS-1) signaling pathway. Previous studies showed that Leukemia related protein 16 (LRP16) reduced insulin stimulated glucose uptake in adipocytes by impairing the IRS-1 signaling pathway. We explored the mechanism by which LRP16 promotes the inflammatory response. Methods: We screened LRP16 induced proteins in the lipopolysaccharide (LPS)-stimulated inflammatory response using liquid chromatography-mass spectrometry (LC-MS) and analyzed the potential biological functions of these proteins using online bioinformatics tools. mRNA expression and protein expression of target genes were measured by real time PCR and Western blot, respectively. Results: A total of 390 differentially expressed proteins were identified. The mitogen-activated protein kinase (MAPK) signaling pathway was the primary activated pathway in LRP16-expressing cells. Overexpression of LRP16 activated ERK1/2 and Rac1, which are two key players related to the MAPK signaling pathway. Furthermore, knock down of endogenous LRP16 by RNA interference (RNAi) reduced Rac1 expression, ERK activation, and inflammatory cytokine expression in human adipocytes stimulated by LPS. The stimulatory effect of LRP16 was diminished by suppressing Rac1 expression and treating the cells with the ERK specific inhibitor, PD98059. Conclusion: These findings revealed the functions of LRP16 in promoting the inflammatory response through activating the Rac1-MAPK1/ERK pathway in human adipocytes.


PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e87030 ◽  
Author(s):  
Yeon-Hui Jeong ◽  
Yongju Kim ◽  
Heebum Song ◽  
Young Sun Chung ◽  
Seung Bum Park ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Yu Li ◽  
Shengnan He ◽  
Jishun Tang ◽  
Nana Ding ◽  
Xiaoyan Chu ◽  
...  

Andrographolide, the main active component extracted from Andrographis paniculata (Burm.f.) Wall. ex Nees, exerts anti-inflammatory effects; however, the principal molecular mechanisms remain unclear. The objective of this study was to investigate the molecular mechanisms of Andrographolide in modifying lipopolysaccharide- (LPS-) induced signaling pathway in RAW264.7 cells. An in vitro model of inflammation was induced by LPS in mouse RAW264.7 cells in the presence of Andrographolide. The concentration and expression levels of proinflammatory cytokines were determined by an enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. The nuclear level of NF-κB was measured by an electrophoretic mobility shift assay (EMSA). The expression levels of NF-κB, p38, ERK, and JNK were determined by western blot. Andrographolide dose-dependently inhibited the release and mRNA expression of TNF-α, IL-6, and IL-1β in LPS-stimulated RAW264.7 cells. The nuclear level of p65 protein was decreased in Andrographolide treatment group. Western blot analysis showed that Andrographolide suppressed LPS-induced NF-κB activation and the phosphorylation of IkBa, ERK1/2, JNK, and p38. These results suggest that Andrographolide exerts an anti-inflammatory effect by inhibiting the activation of NF-κB/MAPK signaling pathway and the induction of proinflammatory cytokines.


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