Inhibition of the pro-inflammatory mediators’ production and anti-inflammatory effect of the iridoid scrovalentinoside

2007 ◽  
Vol 110 (3) ◽  
pp. 419-427 ◽  
Author(s):  
Esperanza Bas ◽  
M. Carmen Recio ◽  
Mohamed Abdallah ◽  
Salvador Máñez ◽  
Rosa M. Giner ◽  
...  
2021 ◽  
Vol 17 (74) ◽  
pp. 275
Author(s):  
Xiaoming CHi ◽  
Xinxin Liang ◽  
Jian Shen ◽  
Xueming Duan ◽  
Rongbing Zhou ◽  
...  

2014 ◽  
Vol 29 (6) ◽  
pp. 117-123
Author(s):  
Gyeong Wi ◽  
Da-Wun Yang ◽  
Ok-Hwa Kang ◽  
Sung-Bae Kim ◽  
Su-Hyun Mun ◽  
...  

2014 ◽  
Vol 42 (04) ◽  
pp. 891-904 ◽  
Author(s):  
Mi Young Song ◽  
Hyo Won Jung ◽  
Seok Yong Kang ◽  
Kyung-Ho Kim ◽  
Yong-Ki Park

The root bark of Lycium barbarum (Lycii radicis cortex, LRC) is used as a cooling agent for fever and night sweats in East Asian traditional medicine. The inhibitory effect of LRC water extract on inflammation is unknown. In this study, the anti-inflammatory effect of LRC was investigated in lipopolysaccharide (LPS)-stimulated mouse macrophage, RAW 264.7 cells. LRC extract significantly decreased the LPS-induced production of inflammatory mediators, nitric oxide (NO), prostaglandin (PG) E2 and pro-inflammatory cytokines, interleukin (IL)-1β and IL-6 in the cells. In addition, LRC extract inhibited the LPS-induced expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 mRNA and protein, and inflammatory cytokines mRNA in the cells. The action mechanism of LRC underlies the blocking of LPS-mediated p38 and Jun N-terminal kinase (JNK), mitogen-activated protein kinases (MAPKs), and the nuclear factor (NF)-κB signaling pathway. These results indicate that LRC extract inhibits the inflammatory response in activated macrophages by down-regulating the transcription levels of inflammatory mediators and blocking the MAPKs and NF-κB pathway.


2017 ◽  
Vol 8 (3) ◽  
pp. 1245-1253 ◽  
Author(s):  
Jau-Tien Lin ◽  
Yuan-Yen Chang ◽  
Yi-Chen Chen ◽  
Bo-Yan Shen ◽  
Deng-Jye Yang

The anti-inflammatory effect and mechanisms ofM. calaburaLinn. fruit.


2020 ◽  
Vol 17 (3) ◽  
pp. 784-825
Author(s):  
Cosmin I. Ciotu ◽  
Michael J. M. Fischer

Abstract A limited number of peripheral targets generate pain. Inflammatory mediators can sensitize these. The review addresses targets acting exclusively or predominantly on sensory neurons, mediators involved in inflammation targeting sensory neurons, and mediators involved in a more general inflammatory process, of which an analgesic effect secondary to an anti-inflammatory effect can be expected. Different approaches to address these systems are discussed, including scavenging proinflammatory mediators, applying anti-inflammatory mediators, and inhibiting proinflammatory or facilitating anti-inflammatory receptors. New approaches are contrasted to established ones; the current stage of progress is mentioned, in particular considering whether there is data from a molecular and cellular level, from animals, or from human trials, including an early stage after a market release. An overview of publication activity is presented, considering a IuPhar/BPS-curated list of targets with restriction to pain-related publications, which was also used to identify topics.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Xiumei Huang ◽  
Bo Li ◽  
Lianzhong Shen

This work is to study the anti-inflammatory effect and its mechanisms of sophoridine in vitro and in vivo. For this aim, the influences of sophoridine on several inflammatory mediators were investigated. Excessive inflammatory response in vitro model was developed by using lipopolysaccharide (LPS) to stimulate the mouse peritoneal macrophages and HL-60 cells to produce IL-6 and IL-8. Carrageenin-induced mouse paw edema model was used as inflammatory response in vivo model. MTT method, ultraviolet spectrophotometric method, and radioimmunoassay were used to measure the changes of TNFα, IL-6, PGE2, and IL-8 in in vitro cell culture supernatant or in the local inflammatory exudates. The results showed that sophoridine inhibited the production of IL-8 in in vitro cell culture supernatant and inhibited the production of TNFα, PGE2, and IL-8 in the local inflammatory exudates but had no significant effects on the production of IL-6 in vitro and in vivo. It is demonstrated that sophoridine’s anti-inflammatory effect was due to its ability to inhibit the production of cytokine and inflammatory mediators.


2019 ◽  
Vol 3 (2) ◽  
pp. 60
Author(s):  
Ami Febriza ◽  
Ridwan Ridwan ◽  
Suryani As'ad ◽  
Vivien Novarina Kasim ◽  
Hasta Handayani Idrus

Obesity is a chronic, low degree systemic inflammatory status. Microarray examination shows a disturbance in the expression of cytokine, chemokine, complementary protein and half of the other acute phase components in obese patients. Adiponectin is the hormone that increases insulin sensitivity, while its level decreases under condition of fatty tissue enlargement that occurs in obesity. Excessive weight causes the adipocyte cells and adipose tissues produce various types of mediators. The inflammatory process is the main cause of metabolic diseases, and the main role of adipose tissue in the inflammatory process is determined by the production of pro-inflammatory mediators and anti-inflammatory mediators. Adiponectin has an important anti-inflammatory effect on obesity. Adiponectin has an important anti-inflammatory effect on obesity. Adiponectin works on macrophage and monocyte to inhibit the production of pro-inflammatory cytokine and increase the expression of interleukin (IL)-10 and IL-1 receptor antagonists. Adiponectin reduces induction of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 endothelial adhesion by TNF-α or resistin. In obese patients, it is characterized by resistance to adiponectin alongside a decrease and the possibility of adiponectin loss in the receptor population in liver and muscles, leading to low adiponectin level.Keywords: adiponectin, obesity, inflammation


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Md Nahidul Islam ◽  
Tomás P. Griffin ◽  
Elizabeth Sander ◽  
Stephanie Rocks ◽  
Junaid Qazi ◽  
...  

Abstract Background Renal proximal tubular epithelial cells (RPTEC) are dysfunctional in diabetic kidney disease (DKD). Mesenchymal stromal cells (MSC) may modulate DKD pathogenesis through anti-inflammatory mediators. This study aimed to investigate the pro-inflammatory effect of extended exposure to high glucose (HG) concentration on stable RPTEC monolayers and the influence of MSC on this response. Methods Morphologically stable human RPTEC/TERT1 cell monolayers were exposed to 5 mM and 30 mM (HG) D-glucose or to 5 mM D-glucose + 25 mM D-mannitol (MAN) for 5 days with sequential immunoassays of supernatants and end-point transcriptomic analysis by RNA sequencing. Under the same conditions, MSC-conditioned media (MSC-CM) or MSC-containing transwells were added for days 4–5. Effects of CM from HG- and MAN-exposed RPTEC/MSC co-cultures on cytokine secretion by monocyte-derived macrophages were determined. Results After 72–80 h, HG resulted in increased RPTEC/TERT1 release of interleukin (IL)-6, IL-8, monocyte chemoattractant protein (MCP)-1 and neutrophil gelatinase-associated lipocalin (NGAL). The HG pro-inflammatory effect was attenuated by concentrated (10×) MSC-CM and, to a greater extent, by MSC transwell co-culture. Bioinformatics analysis of RNA sequencing data confirmed a predominant effect of HG on inflammation-related mediators and biological processes/KEGG pathways in RPTEC/TERT1 stable monolayers as well as the non-contact-dependent anti-inflammatory effect of MSC. Finally, CM from HG-exposed RPTEC/MSC transwell co-cultures was associated with attenuated secretion of inflammatory mediators by macrophages compared to CM from HG-stimulated RPTEC alone. Conclusions Stable RPTEC monolayers demonstrate delayed pro-inflammatory response to HG that is attenuated by close proximity to human MSC. In DKD, this MSC effect has potential to modulate hyperglycemia-associated RPTEC/macrophage cross-talk.


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