Protective effects of orally administered shark compound peptides from Chiloscyllium plagiosum against acute inflammation

2021 ◽  
Vol 45 (2) ◽  
Author(s):  
Tong‐Xin Wang ◽  
Dong‐Yan Shen ◽  
Qin Wang ◽  
Xin‐Heng Xu ◽  
Xi Wang ◽  
...  
2017 ◽  
Vol 115 ◽  
pp. 255-266 ◽  
Author(s):  
L. Rodrigues ◽  
E. Ekundi-Valentim ◽  
J. Florenzano ◽  
A.R.A. Cerqueira ◽  
A.G. Soares ◽  
...  

2015 ◽  
Vol 69 (9) ◽  
Author(s):  
Dominika Topoľská ◽  
Katarína Valachová ◽  
Peter Rapta ◽  
Stanislav Šilhár ◽  
Elena Panghyová ◽  
...  

AbstractPotential protective effects of elderberry (Sambucus nigra) extracts against oxidative degradation of hyaluronan (HA) were detected in vitro. To induce free-radical-mediated HA degradation, Weissberger’s biogenic oxidative system, which mimics the situation of acute inflammation, was applied. Time- and dose-dependent changes of dynamic viscosity of the HA solutions in the presence and absence of two elderberry extracts produced in 2006 and 2012 were recorded by rotational viscometry (RV). Radical scavenging capacity of both extracts was investigated by the spectrocolorimetric ABTS [2,2′-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt] assay and the “inverted” ABTS assay. Oxygen consumption of the system oxidizing HA either in the absence or presence of the elderberry extracts was determined. The results of RV revealed that an addition of the newer extract (2012) promoted the inhibition of HA degradation more markedly compared to the older extract (2006). The same effect of both extracts on ABTS


2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Fangfang Bi ◽  
Wenbo Liu ◽  
Zongtao Wu ◽  
Chen Ji ◽  
Cuicui Chang

Antiaging protein Klotho exhibits impressive properties of anti-inflammation, however is declined early after intervertebral disc injury, making Klotho restoration an attractive strategy of treating intervertebral disc inflammatory disorders. Here, we have found that Klotho is enriched in nucleus pulposus (NP) cells and Klotho overexpression attenuates H2O2-induced acute inflammation essentially via suppressing Toll-like receptor 4 (TLR4). The proinflammatory NF-κB signaling and cytokine expressions paralleled with Klotho repression and TLR4 elevation in both NP cells (H2O2 treatment) and rat intervertebral disc (needle puncture treatment). Overexpression of TLR4 downregulated expression of Klotho, whereas interfering TLR4 expression diminished the inhibitory effects of H2O2 on Klotho in NP cells. Consistently, Klotho knockdown by RNA interferences largely diminished the anti-inflammatory and intervertebral disc protective effects in an Intervertebral Disc Degeneration (IDD) model. Thus, our study indicates that TLR4-NF-κB signaling and Klotho form a negative-feedback loop in NP cells. Also, we demonstrate that the expression of Klotho is regulated by the balance between upregulation and downregulation of TLR4-NF-κB signaling.


Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 859
Author(s):  
Jung-Seop Lee ◽  
In-ho Song ◽  
Pramod B. Shinde ◽  
Satish Balasaheb Nimse

Oxidative stress due to the high levels of reactive oxygen species (ROS) that damage biomolecules (lipids, proteins, DNA) results in acute inflammation. However, without proper intervention, acute inflammation progresses to chronic inflammation and then to several chronic diseases, including cancer, myocardial infarction, cardiovascular diseases, chronic inflammation, atherosclerosis, and more. There has been extensive research on the antioxidants of natural origin. However, there are myriad possibilities for the development of synthetic antioxidants for pharmacological applications. There is an increasing interest in the identification of novel synthetic antioxidants for the modulation of biochemical processes related to ROS. In this regard, derivatives of supramolecules, such as calix[n]arene, resorcinarene, calixtyrosol, calixpyrrole, cucurbit[n]uril, porphyrin etc. are gaining attention for their abilities to scavenge the free radicals. Supramolecular chemistry offers excellent scaffolds for the development of novel antioxidants that can be used to modulate free radical reactions and to improve the disorders related to oxidative stress. This review focuses on the interdisciplinary approach for the design and development of novel synthetic antioxidants based on supramolecular scaffolds, with potentially protective effects against oxidative stress.


2016 ◽  
Vol 83 ◽  
pp. 1191-1202 ◽  
Author(s):  
Maria-Eduardo Figueira ◽  
Mónica Oliveira ◽  
Rosa Direito ◽  
João Rocha ◽  
Paula Alves ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Toru Kusano ◽  
Kuei-Chen Chiang ◽  
Masafumi Inomata ◽  
Yayoi Shimada ◽  
Naoya Ohmori ◽  
...  

Background. Histones play important roles in both host defenses and inflammation related to microbial infection. A peptide mimotope (SSV) was identified from a novel histone H1 monoclonal antibody (16G9 mAb) that was shown to inhibit the mixed lymphocyte reaction. In the present study, an anti-SSV producing hybridoma was established. We investigated the effects of SSV mAb in a mouse acute inflammation model induced by intraperitoneal injection of lipopolysaccharide (LPS).Methods. SSV mAb was generated and characterized. Mice were treated with SSV mAb or a control IgG antibody prior to LPS injection. Evaluation of survival rate and lung tissue on histological score was performed. The levels of inflammatory cytokines and histones H1, H3, and H4 in plasma and lung tissue were measured by ELISA.Results. Competitive ELISA revealed that SSV mAb binds to histone H1. SSV mAb improved lung injury and prolonged the survival of LPS-injected mice. Increased levels of histones H1, H3, and H4 and inflammatory cytokines (TNF-α, IL-1β, and IL-6) in plasma and lung tissue after LPS injection were ameliorated by SSV mAb.Conclusion. SSV mAb is shown to have anti-inflammatory activity and organ-protective effects, highlighting the importance of controlling histone H1 as well as H3 and H4 levels during inflammation.


2017 ◽  
Vol 6 (2) ◽  
pp. 78-81 ◽  
Author(s):  
Ali Audu Jigam ◽  
◽  
Fatima Mahmood ◽  
Bashir Lawal ◽  
◽  
...  

2021 ◽  
Vol 22 (24) ◽  
pp. 13576
Author(s):  
Kristian-Christos Ngamsri ◽  
Rizki A. Putri ◽  
Christoph Jans ◽  
Katharina Schindler ◽  
Anika Fuhr ◽  
...  

Peritonitis and peritonitis-associated sepsis are characterized by an increased formation of platelet–neutrophil complexes (PNCs), which contribute to an excessive migration of polymorphonuclear neutrophils (PMN) into the inflamed tissue. An important neutrophilic mechanism to capture and kill invading pathogens is the formation of neutrophil extracellular traps (NETs). Formation of PNCs and NETs are essential to eliminate pathogens, but also lead to aggravated tissue damage. The chemokine receptors CXCR4 and CXCR7 on platelets and PMNs have been shown to play a pivotal role in inflammation. Thereby, CXCR4 and CXCR7 were linked with functional adenosine A2B receptor (Adora2b) signaling. We evaluated the effects of selective CXCR4 and CXCR7 inhibition on PNCs and NETs in zymosan- and fecal-induced sepsis. We determined the formation of PNCs in the blood and, in addition, their infiltration into various organs in wild-type and Adora2b−/− mice by flow cytometry and histological methods. Further, we evaluated NET formation in both mouse lines and the impact of Adora2b signaling on it. We hypothesized that the protective effects of CXCR4 and CXCR7 antagonism on PNC and NET formation are linked with Adora2b signaling. We observed an elevated CXCR4 and CXCR7 expression in circulating platelets and PMNs during acute inflammation. Specific CXCR4 and CXCR7 inhibition reduced PNC formation in the blood, respectively, in the peritoneal, lung, and liver tissue in wild-type mice, while no protective anti-inflammatory effects were observed in Adora2b−/− animals. In vitro, CXCR4 and CXCR7 antagonism dampened PNC and NET formation with human platelets and PMNs, confirming our in vivo data. In conclusion, our study reveals new protective aspects of the pharmacological modulation of CXCR4 and CXCR7 on PNC and NET formation during acute inflammation.


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