- |||||||||| Journal: Activation of ROS/MAPKs/NF-κB/NLRP3 and inhibition of efferocytosis in osteoclast-mediated diabetic osteoporosis. (Pubmed Central) - May 27, 2020
In streptozotocin-induced diabetic rats in vivo, the numbers and the bone-resorption capacity of OCs as well as the serum levels of TRACP-5b were significantly increased, and the expression of MAPK-, NF-κB-, and NLRP3 inflammasome-related proteins in the proximal tibia were also significantly elevated; however, treatment with insulin and LXA4 reversed this elevation. Together, these results demonstrated that the activation of ROS/MAPKs/NF-κB/NLRP3 and the inhibition of efferocytosis in OCs are the main causes of osteoporosis in DM.-An, Y., Zhang, H., Wang, C., Jiao, F., Xu, H., Wang, X., Luan, W., Ma, F., Ni, L., Tang, X., Liu, M., Guo, W., Yu, L. Activation of ROS/MAPKs/NF-κB/NLRP3 and inhibition of efferocytosis in osteoclast-mediated diabetic osteoporosis.
- |||||||||| Preclinical, Journal, IO Biomarker: S-allyl cysteine, an active ingredient of garlic, attenuates acute liver dysfunction induced by lipopolysaccharide/ d-galactosamine in mouse: Underlying mechanisms. (Pubmed Central) - May 27, 2020
Additionally, SAC was capable to ameliorate apoptotic biomarkers including caspase 3 and DNA fragmentation. In summary, SAC can protect liver against LPS/d-Gal by attenuation of neutrophil infiltration, oxidative stress, inflammation, apoptosis, and pyroptosis which is partly linked to its suppression of TLR4/NF-κB/NLRP3 signaling.
- |||||||||| colchicine / Generic mfg.
Journal: Colchicine inhibits endothelial inflammation via NLRP3/CRP pathway. (Pubmed Central) - May 26, 2020 In summary, SAC can protect liver against LPS/d-Gal by attenuation of neutrophil infiltration, oxidative stress, inflammation, apoptosis, and pyroptosis which is partly linked to its suppression of TLR4/NF-κB/NLRP3 signaling. No abstract available
- |||||||||| Journal: Carbon nanotubes and crystalline silica stimulate robust ROS production, inflammasome activation, and IL-1β secretion in macrophages to induce myofibroblast transformation. (Pubmed Central) - May 25, 2020
Induction of IL-1β is dependent on the activation of the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome and ROS (reactive oxygen species) production in macrophages, as inhibition of NLRP3 by MCC950 and reduction of ROS production by N-acetylcysteine blocked NLRP3 activation, IL-1β induction, and fibroblast activation and differentiation. Therefore, fibrogenic CNTs and silica, but not CB, elicit robust macrophage-guided myofibroblast transformation, which depends on the induction of IL-1β through the NLRP3 inflammasome pathway and the increased production of ROS in macrophages.
- |||||||||| tamoxifen / Generic mfg.
Preclinical, Journal: NLRP3 inflammasome activation in hepatic stellate cells induces murine liver fibrosis. (Pubmed Central) - May 23, 2020 Primary HSCs isolated from wild-type (WT), Nlrp3 , or Nlrp3 knock-in crossed to inducible (estrogen receptor Cre-CreT) mice were incubated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP), or 4OH-tamoxifen, respectively...Liver sections from 24 week-old Nlrp Lrat Cre mice showed fibrotic changes with increased αSMA and desmin positive cells and collagen deposition, independent of inflammatory infiltrates; these changes were also observed after LPS challenge in 8 week-old Nlrp Lrat Cre mice. Conclusion Our results highlight a direct role for the NLRP3 inflammasome in the activation of HSC directly triggering liver fibrosis.
- |||||||||| Review, Journal: Reactive species-induced microvascular dysfunction in ischemia/reperfusion. (Pubmed Central) - May 23, 2020
On the other hand, RS production at signaling levels promotes ischemic angiogenesis, mediates flow-induced dilation in patients with coronary artery disease, and instigates the activation of cell survival programs by conditioning stimuli that render tissues resistant to the deleterious effects of prolonged I/R. These topics will be reviewed in this article.
- |||||||||| Journal: Severe acute respiratory syndrome coronavirus ORF3a protein activates the NLRP3 inflammasome by promoting TRAF3-dependent ubiquitination of ASC. (Pubmed Central) - May 23, 2020
Taken together, our findings reveal a new mechanism by which SARS-CoV ORF3a protein activates NF-κB and the NLRP3 inflammasome by promoting TRAF3-dependent ubiquitination of p105 and ASC.-Siu, K.-L., Yuen, K.-S., Castaño-Rodriguez, C., Ye, Z.-W., Yeung, M.-L., Fung, S.-Y., Yuan, S., Chan, C.-P., Yuen, K.-Y., Enjuanes, L., Jin, D.-Y. Severe acute respiratory syndrome coronavirus ORF3a protein activates the NLRP3 inflammasome by promoting TRAF3-dependent ubiquitination of ASC.
- |||||||||| Decadron (dexamethasone) / Merck (MSD)
Journal: Contribution of cathepsin B-dependent Nlrp3 inflammasome activation to nicotine-induced endothelial barrier dysfunction. (Pubmed Central) - May 23, 2020 Collectively, our data suggest that nicotine enhances cathepsin B-dependent Nlrp3 inflammasome activation and the consequent production of a novel permeability factor HMGB1, which causes disruption of inter-endothelial tight junctions leading to endothelial hyperpermeability. Instigation of endothelial inflammasomes may serve as an important pathogenic mechanism contributing to the early onset of vasculopathy associated with smoking.
- |||||||||| colchicine / Generic mfg., Ilaris (canakinumab) / Novartis
[VIRTUAL] CLINICAL FEATURES AND ANALYSIS OF MEFV GENE IN 31 PATIENTS WITH FAMILIAL MEDITERRANEAN FEVER (FMF) () - May 22, 2020 - Abstract #EULAR2020EULAR_3227; We have examined association between clinical features and mutations of MEFV in 31 patients in Gifu district, suggesting that duration of fever attacks and frequency of fever attacks in G1 are significantly shorter than G2 and G3, respectively in Japanese patients with FMF. Mutations of E148Q in exon 2 were observed in 16-23 % of normal Japanese patients, indicating that E148Q is the polymorphism or accelerating factor.
- |||||||||| lenabasum (JBT-101) / Corbus Pharma, Kaken
[VIRTUAL] LENABASUM, A CB2 AGONIST, INHIBITS INFLAMMASOME ACTIVATION () - May 22, 2020 - Abstract #EULAR2020EULAR_1633; Our data revealed that Ala 348 to Thr up-regulate the functional status of P2X7R and Glu 496 to Ala and Gln 460 to Arg down-regulate the functional status of P2X7R, which resulted in a significant increase or decrease in IL-1β and NLRP3 expression levels with high uric acid. Lenabasum inhibits inflammasome activation, which could contribute to potential therapeutic efficacy in SSc and other autoimmune diseases.
- |||||||||| Journal: Design, synthesis, and screening of sulfonylurea-derived NLRP3 inflammasome inhibitors. (Pubmed Central) - May 22, 2020
The polar enone functional alert of chalcone was replaced with a sulfonylurea scaffold while maintaining the relative positions of the two aromatic rings. These compounds were evaluated for their ability to inhibit NLRP3 and AIM2 inflammasome activation triggered by Francisella tularensis infection.
- |||||||||| low molecular weight dextran sulfate (ILB) / TikoMed
Journal: Caffeic Acid Phenethyl Ester Prevents Colitis-Associated Cancer by Inhibiting NLRP3 Inflammasome. (Pubmed Central) - May 22, 2020 Here, we aimed to evaluate the anti-inflammatory effect of caffeic acid phenethyl ester (CAPE) on bone marrow-derived macrophages (BMDMs), THP-1 cells, and azoxymethane/dextran sulfate sodium (AOM/DSS)-induced colon cancer mouse model...Altogether, our findings demonstrate that CAPE prevents CAC by post-transcriptionally inhibiting NLRP3 inflammasome. Thus, CAPE may be an effective candidate for reducing the risk of CAC in patients with inflammatory bowel disease.
- |||||||||| Journal: Zearalenone induces NLRP3-dependent pyroptosis via activation of NF-κB modulated by autophagy in INS-1 cells. (Pubmed Central) - May 21, 2020
Furthermore, we indicated that ZEA-induced NF-κB p65 activation contributed to the activation of the NLRP3 inflammasome, inflammatory response, and pyroptosis in INS-1 cells, which were indicated by western blot and immunofluorescence, and the activation of NF-κB p65 induced by ZEA was autophagy-dependent. This study demonstrates that ZEA induces NLRP3-dependent pyroptosis via activation of NF-κB modulated by autophagy in INS-1 cells.
- |||||||||| [VIRTUAL] Non Targeting Locked Nucleic Acids Antagonize Inflammatory Activation of Foam Cells and Impede Atherosclerosis () - May 20, 2020 - Abstract #ATVBPVDGPM2020ATVB_PVD_GPM_103;
Moreover, differential expression analysis of leukocyte populations revealed blunted expression of inflammatory mediators (Il1b, Nlrp3, Tnf), oxidative stress (Mpo, Sod2, Ptgs2), and extracellular matrix remodeling genes (Mmp9, Prtn3, Elane). Taken together, our results put forth a novel paradigm in which sRNA-cargo of LDL promote inflammatory activation of macrophages in the artery wall and identify TLR8 antagonism with ntLNA as a viable strategy for the treatment of chronic inflammation in CVD.
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