Assays for macrophage inflammatory proteins

Author(s):  
Anne-Marie Buckle ◽  
Stewart Craig ◽  
Lloyd G. Czaplewski
Author(s):  
Umme Hani ◽  
Shivananda Kandagalla ◽  
B.S. Sharath ◽  
K Jyothsna. ◽  
H Manjunatha.

: Hsp90 are molecular chaperones of chronic inflammatory proteins and have emerged as prime target for treatment of inflammation. Principal components from Curcuma longa and Camellia sinensis, Curcumin and EGC respectively possesses anti-inflammatory properties inhibiting cytokines responsible for inflammation. Both act on common pathways in upregulation of heme oxygenase 1 through Pkcδ-Nrf2 pathway and downregulation of Tlr4, which in turn suppress expression of Hsp90. Curcumin and EGC were also found to bind -N and -C terminal domain of Hsp90 respectively. Based on this, work was designed with network pharmacological approach. Hsp90 associated gene targets of Curcumin and EGC were collected from databases, and gene ontology studies were done. PPI were obtained from string database for specific genes involved in Pkcδ-Nrf2 and Tlr4 pathway. Protein interaction network was constructed by cytoscape, and networks of Hsp90, Curcumin and EGC were merged to get common genes involved in Pkcδ-Nrf2 and Tlr4 pathway. Cluego analysis was done for obtained common genes to identify functional behavior in human diseases. Main proteins involved were identified as key regulators in Pkcδ-Nrf2 and Tlr4 pathway for controlling expression of Hsp90 from Curcumin and EGC in inflammation. Docking was performed on main proteins, Hsp90, Pkcδ and Tlr4 with Curcumin and EGC, significant binding energy was obtained for docked complexes. Combinatorial effects of Curcumin and EGC were observed in Pkcδ-Nrf2 and Tlr4pathway. Present study is an attempt to unravel common pathways mediated in intervention of Curcumin and EGC for suppression of Hsp90 associated with inflammation.


2016 ◽  
Vol 34 (7) ◽  
pp. 305-312 ◽  
Author(s):  
Marta Łukaszewicz-Zając ◽  
Maciej Szmitkowski ◽  
Ala Litman-Zawadzka ◽  
Barbara Mroczko

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 743
Author(s):  
Chao Yu Hsu ◽  
Yi Sheng Lin ◽  
Wei Chun Weng ◽  
Lauren Panny ◽  
Hsiang Lai Chen ◽  
...  

The inflammatory process is proposed to be one of the factors to benign prostatic enlargement (BPH), and this is the first study examining the anti-inflammatory ability of phloretin in treating rats with testosterone-induced BPH. BPH would be induced by testosterone (10 mg/kg/day testosterone subcutaneously for 28 days), and the other groups of rats were treated with phloretin 50 mg/kg/day or 100 mg/kg/day orally (phr50 or phr100 group) after induction. Prostate weight and prostate weight to body weight ratio were significantly reduced in the Phr100 group. Reduced dihydrotestosterone without interfering with 5α-reductase was observed in the phr100 group. In inflammatory proteins, reduced IL-6, IL-8, IL-17, NF-κB, and COX-2 were seen in the phr100 group. In reactive oxygen species, malondialdehyde was reduced, and superoxide dismutase and glutathione peroxidase were elevated in the phr100 group. In apoptotic assessment, elevated cleaved caspase-3 was observed in rats of the phr100 group. Enhanced pro-apoptotic Bax and reduced anti-apoptotic Bc1-2 could be seen in the phr100 group. In histological stains, markedly decreased glandular hyperplasia and proliferative cell nuclear antigen were observed with reduced expression in the phr100 group. Meanwhile, positive cells of terminal deoxynucleotidyl transferase dUTP nick end labeling were increased in the phr100 group. In conclusion, the treatment of phloretin 100 mg/kg/day could ameliorate testosterone-induced BPH.


Burns ◽  
2021 ◽  
Author(s):  
Yongqiang Zhou ◽  
Helv Yan ◽  
Ting Li ◽  
Mei Xie ◽  
Xiuya Li ◽  
...  

2021 ◽  
Vol 2 (1) ◽  
pp. 108-119
Author(s):  
Hans O. Kalkman

Mutations in the genes coding for tryptophan-hydrolase-2 and the scaffold protein FKBP5 are associated with an increased risk of suicide. The mutation in both cases enhances the enzymatic activity of glycogen synthase kinase-3 (GSK3). Conversely, anti-suicidal medications, such as lithium, clozapine, and ketamine, indirectly inhibit the activity of GSK3. When GSK3 is active, it promotes the metabolic removal of the transcription factor NRF2 (nuclear factor erythroid 2-related factor-2), which suppresses the transcription of multiple genes that encode anti-oxidative and anti-inflammatory proteins. Notably, several suicide-biomarkers bear witness to an ongoing inflammatory process. Moreover, alterations in serum lipid levels measured in suicidal individuals are mirrored by data obtained in mice with genetic deletion of the NRF2 gene. Inflammation is presumably causally related to both dysphoria and anger, two factors relevant for suicide ideation and attempt. Preventing the catabolism of NRF2 could be a strategy to obtain novel suicide-prophylactic medications. Possible candidates are minocycline and nicotinic-α7 agonists. The antibiotic minocycline indirectly activates NRF2-transcriptional activity, whereas the activation of nicotinic-α7 receptors indirectly inhibits GSK3.


Author(s):  
Chinedu C. Ude ◽  
Shiv Shah ◽  
Kenneth S. Ogueri ◽  
Lakshmi S. Nair ◽  
Cato T. Laurencin

Abstract Purpose The knee joint is prone to osteoarthritis (OA) due to its anatomical position, and several reports have implicated the imbalance between catabolic and anabolic processes within the joint as the main culprit, thus leading to investigations towards attenuation of these inflammatory signals for OA treatment. In this review, we have explored clinical evidence supporting the use of stromal vascular fraction (SVF), known for its anti-inflammatory characteristics for the treatment of OA. Methods Searches were made on PubMed, PMC, and Google Scholar with the keywords “adipose fraction knee regeneration, and stromal vascular fraction knee regeneration, and limiting searches within 2017–2020. Results Frequently found interventions include cultured adipose-derived stem cells (ADSCs), SVF, and the micronized/microfragmented adipose tissue-stromal vascular fraction (MAT-SVF). Clinical data reported that joints treated with SVF provided a better quality of life to patients. Currently, MAT-SVF obtained and administered at the point of care is approved by the Food and Drug Administration (FDA), but more studies including manufacturing validation, safety, and proof of pharmacological activity are needed for SVF. The mechanism of action of MAT-SVF is also not fully understood. However, the current hypothesis indicates a direct adherence and integration with the degenerative host tissue, and/or trophic effects resulting from the secretome of constituent cells. Conclusion Our review of the literature on stromal vascular fraction and related therapy use has found evidence of efficacy in results. More research and clinical patient follow-up are needed to determine the proper place of these therapies in the treatment of osteoarthritis of the knee. Lay Summary Reports have implicated the increased inflammatory proteins within the joints as the main cause of osteoarthritis (OA). This has attracted interest towards addressing these inflammatory proteins as a way of treatment for OA. The concentrated cell-packed portion of the adipose product stromal vascular fraction (SVF) from liposuction or other methods possesses anti-inflammatory effects and has been acclaimed to heal OA. Thus, we searched for clinical evidence supporting their use, for OA treatment through examining the literature. Data from various hospitals support that joints treated with SVF provided a better quality of life to patients. Currently, there is at least one version of these products that are obtained and given back to patients during a single clinic visit, approved by the FDA.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Zaipul I. Md Dom ◽  
Caterina Pipino ◽  
Bozena Krolewski ◽  
Kristina O’Neil ◽  
Eiichiro Satake ◽  
...  

AbstractWe recently identified a kidney risk inflammatory signature (KRIS), comprising 6 TNF receptors (including TNFR1 and TNFR2) and 11 inflammatory proteins. Elevated levels of these proteins in circulation were strongly associated with risk of the development of end-stage kidney disease (ESKD) during 10-year follow-up. It has been hypothesized that elevated levels of these proteins in circulation might reflect (be markers of) systemic exposure to TNFα. In this in vitro study, we examined intracellular and extracellular levels of these proteins in human umbilical vein endothelial cells (HUVECs) exposed to TNFα in the presence of hyperglycemia. KRIS proteins as well as 1300 other proteins were measured using the SOMAscan proteomics platform. Four KRIS proteins (including TNFR1) were down-regulated and only 1 protein (IL18R1) was up-regulated in the extracellular fraction of TNFα-stimulated HUVECs. In the intracellular fraction, one KRIS protein was down-regulated (CCL14) and 1 protein was up-regulated (IL18R1). The levels of other KRIS proteins were not affected by exposure to TNFα. HUVECs exposed to a hyperglycemic and inflammatory environment also showed significant up-regulation of a distinct set of 53 proteins (mainly in extracellular fraction). In our previous study, circulating levels of these proteins were not associated with progression to ESKD in diabetes.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Lillemor Berntson

Abstract Background To explore possible anti-inflammatory effects of the specific carbohydrate diet in children with juvenile idiopathic arthritis. This diet has shown anti-inflammatory effect in children with inflammatory bowel disease. Methods Twenty-two patients with juvenile idiopathic arthritis (age 6.3–17.3 years), with ≤2 inflamed joints and an erythrocyte sedimentation rate < 30 mm/h, were included in this explorative study. Fifteen children completing four weeks on the diet were evaluated. A dietician introduced parents and children to the diet, and two follow-ups were performed during the intervention. Conventional laboratory tests and multiplex analyses of 92 inflammatory proteins were used. Short-chain fatty acids in faecal samples were examined. Results The diet significantly decreased morning stiffness (p = 0.003) and pain (p = 0.048). Physical function, assessed through the child health assessment questionnaire, improved (p = 0.022). Arthritis improved in five of the seven children with arthritis; in those seven, multiplex analyses showed a significant decrease in nine inflammatory proteins, including TNF-alpha (p = 0.028), after four weeks. Faecal butyrate, analysed in all 15 participants, increased significantly (p = 0.020). Conclusion The specific carbohydrate diet may have significant positive effects on arthritis in children with juvenile idiopathic arthritis, but further studies are needed. Clinical trials identifier NCT04205500, 2019/12/17, retrospectively registered. URL: https://register.clinicaltrials.gov


2008 ◽  
Vol 162 (5) ◽  
pp. 462 ◽  
Author(s):  
Jonatan R. Ruiz ◽  
Francisco B. Ortega ◽  
Julia Wärnberg ◽  
Luis A. Moreno ◽  
Juan J. Carrero ◽  
...  

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