NLRP3 inhib 
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  • ||||||||||  Journal:  Inhibition of NLRP3 inflammasome activation on the inflammatory response of macrophage induced by silica dust (Pubmed Central) -  Nov 2, 2020   
    Compared with the NLRP3 inhibitor group, the IL-1β level of NR8383 cells in luteolin group decreased significantly at 12, 24 and 48 h, the IL-18 and TGF-β1 levels decreased significantly at 48 h, the NLRP3 and Caspase-1 levels decreased significantly at 24 h (P<0.05) . Inhibition of NLRP3 inflammaasome activation can reduce the inflammatory response of macrophages induced by SiO(2) dust.
  • ||||||||||  Reasanz (serelaxin) / Novartis
    Journal:  H3 relaxin protects against calcium oxalate crystal-induced renal inflammatory pyroptosis. (Pubmed Central) -  Nov 1, 2020   
    Inhibition of NLRP3 inflammaasome activation can reduce the inflammatory response of macrophages induced by SiO(2) dust. Our results provide previously unidentified mechanistic insights into CaOx crystal-induced inflammatory pyroptotic damage and H3 relaxin-mediated anti-inflammatory protection and thus suggest a series of potential therapeutic targets and methods for but not limited to nephrocalcinosis.
  • ||||||||||  Clinical, Journal:  Expression and Clinical Prognostic Value of Platelet NLRP3 in Acute Coronary Syndrome. (Pubmed Central) -  Nov 1, 2020   
    Moreover, the NLRP3-high group exhibited higher platelet activity, as indicated by increased PAC-1 binding and CD62P expression, compared with the NLRP3-low group (P<0.001). These results indicated that platelet NLRP3 was a novel potential prognostic factor for patients with ACS that underwent PCI.
  • ||||||||||  Journal:  Evaluation of Canonical Inflammasome Activation in Human Monocytes by Imaging Flow Cytometry. (Pubmed Central) -  Oct 31, 2020   
    By applying these tools in PBMCs from patients with distinct inflammatory disorders we demonstrate that MIFC is able to assess canonical inflammasome activation in a quantitative and statistically robust manner in clinically relevant samples. Therefore, we propose that accurate assessment of specks by MIFC could help guide preventive or therapeutic strategies in an array of human inflammatory diseases in which inflammasomes play an important role.
  • ||||||||||  MPE-001 / Mperia Therapeutics
    Journal, IO Biomarker:  Immunometabolic modulation of retinal inflammation by CD36 ligand. (Pubmed Central) -  Oct 30, 2020   
    Accordingly, PPAR-γ inhibition blocked the cytoprotective effect of MPE-001 on photoreceptor apoptosis elicited by activated MP. By altering activated MP metabolism, MPE-001 decreased immune responses to alleviate subsequent inflammation-dependent neuronal injury characteristic of various vision-threatening retinal disorders.
  • ||||||||||  Journal:  Signaling pathways that regulate Trypanosoma cruzi infection and immune response. (Pubmed Central) -  Oct 30, 2020   
    On the other hand, the modulation of macrophage activation may be instrumental in allowing parasite persistence and long-term host survival. In this sense, we discuss the importance of the metabolism of two amino acids: L-arginine and tryptophan, and evaluate the role of iNOS, arginase and IDO enzymes in the regulation of innate and adaptive immune response during this infection; and, finally, we also discuss how T. cruzi exploits the AhR, mTOR and Wnt signaling pathways to promote their intracellular replication in macrophages, thus evading the host's immune response.
  • ||||||||||  Preclinical, Journal:  Kellerin alleviates cognitive impairment in mice after ischemic stroke by multiple mechanisms. (Pubmed Central) -  Oct 30, 2020   
    Moreover, in in vitro studies, we found that kellerin regulated microglial polarization and inhibited the NLRP3 and MAPK signaling pathways after LPS treatment. These findings provide a new understanding of the function of kellerin in ischemic stroke, and suggest that kellerin could be a potential therapeutic agent for the treatment of ischemic stroke.
  • ||||||||||  Review, Journal:  Statins: Could an old friend help the fight against COVID-19? (Pubmed Central) -  Oct 30, 2020   
    The well-known anti-inflammatory properties of statins, by blocking several molecular mechanisms, including NF-κB and NLRP3 inflammasome, could limit the "cytokine storm" in severe COVID-19 patients which is linked to fatal outcome. Finally, statin moderation of coagulation response activation may also contribute to improve COVID-19 outcomes.
  • ||||||||||  Journal:  Identification of a Novel Orally Bioavailable NLRP3 Inflammasome Inhibitor. (Pubmed Central) -  Oct 30, 2020   
    In this study, rationally designed alkenyl sulfonylurea derivatives were identified as novel, potent and orally bioavailable NLRP3 inhibitors. Compound 7 was found to be potent (IL-1β IC = 35 nM; IL-18 IC = 33 nM) and selective NLRP3 inflammasome inhibitor with excellent pharmacokinetic profile having oral bioavailability of 99% in mice.
  • ||||||||||  Journal:  Resolvin D1 alleviates cerebral ischemia/reperfusion injury in rats by inhibiting NLRP3 signaling pathway. (Pubmed Central) -  Oct 30, 2020   
    Furthermore, it was discovered that RvD1 repressed the protein expression of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) in the brain tissues of rats with I/R injury (P<0.05). The protective effect of RvD1 on the rats against cerebral I/R injury may be related to its inhibition on NLRP3 inflammasome, and RvD1 is expected to become a targeted drug for the clinical treatment of cerebral I/R injury.
  • ||||||||||  Actemra IV (tocilizumab) / Roche, JW Pharma
    Clinical, Review, Journal:  Immunomodulatory Therapies for COVID-19 in Solid Organ Transplant Recipients. (Pubmed Central) -  Oct 30, 2020   
    A number of case reports, case series, and non-controlled cohort studies have assessed the efficacy and safety of the anti-IL-6-receptor monoclonal tocilizumab in SOT (namely kidney transplantation) recipients with COVID-19 pneumonia and CRS...Anecdotal experiences have been reported with the use of the anti-IL-1 agent anakinra and the NLRP3 inflammasome inhibitor colchicine in this population...However, the supporting evidence is scarce and of low quality. In the absence of RCT, observational studies including well-matched control groups should be designed in future.
  • ||||||||||  Journal:  Crucial Role of NLRP3 Inflammasome in the Development of Peritoneal Dialysis-related Peritoneal Fibrosis. (Pubmed Central) -  Oct 28, 2020   
    Furthermore, in vitro experiments showed that MGO induced cell death via the generation of reactive oxygen species in vascular endothelial cells, which was inhibited by ASC deficiency. Our results showed that endothelial NLRP3 inflammasome contributes to PD-related peritoneal inflammation and fibrosis, and provide new insights into the mechanisms underlying the pathogenesis of this disorder.
  • ||||||||||  Journal:  Effects of XIAP on high fat diet-induced hepatic steatosis: a mechanism involving NLRP3 inflammasome and oxidative stress. (Pubmed Central) -  Oct 28, 2020   
    In contrast, overexpression of XIAP by transfection in vitro restrained PA-stimulated hepatic steatosis by suppression of oxidative stress, NLRP3 related inflammatory response, and impairment of Nrf2 activity, further alleviating abnormal metabolic disorder associated NAFLD. Taken together, the present study helped to elucidate how HFD-induced hepatic steatosis was regulated by XIAP, possibly via the inhibition of NLRP3 signaling and oxidative stress injury.
  • ||||||||||  everolimus / Generic mfg., sirolimus / Generic mfg.
    Journal:  Statins activate the NLRP3 inflammasome and impair insulin signalling via p38 and mTOR. (Pubmed Central) -  Oct 28, 2020   
    Rapamycin (20 nM) or the rapalog, Everolimus (20 nM) prevented atorvastatin-induced lowering of insulin-mediated phosphorylation of Akt in mouse adipose tissue. These results position p38 and mTOR as mediators of statin-induced insulin resistance in adipose tissue and highlight rapalogs as candidates to mitigate the insulin resistance and glycemic side effects of statins.
  • ||||||||||  Clinical, Journal:  Differential Immune Activation in Fetal Macrophage Populations. (Pubmed Central) -  Oct 27, 2020   
    Our data show that CD11b macrophages derived from fetal liver are the major pro-inflammatory cells in the developing fetus. These findings could have important implications in better understanding the fetal inflammatory response and the unique features of neonatal immunity.
  • ||||||||||  Biomarker, Clinical, Journal:  Circulatory miR-223-3p Discriminates Between Parkinson's and Alzheimer's Patients. (Pubmed Central) -  Oct 27, 2020   
    Receiver operating characteristic analysis showed that miR-223-3p concentration discriminates between AD, PD and MCI vs. HC, as well as between AD and PD. miR-223-3p serum concentration discriminates between AD/MCI and PD, suggesting that this molecule could be a potential non-invasive biomarker for differential diagnosis and prognosis of these neurodegenerative conditions.
  • ||||||||||  Preclinical, Journal:  Fraxin inhibits lipopolysaccharide-induced inflammatory cytokines and protects against endotoxic shock in mice. (Pubmed Central) -  Oct 27, 2020   
    Western blot assay demonstrated that the pretreatment with fraxin could down-regulate LPS-induced protein expressions of NF-?B and NLRP3 inflammatory corpuscle signalling pathways. Overall, fraxin had protective effects on LPS-induced endotoxic shock mice and the possible mechanisms might through activating NF-?B and NLRP3 inflammatory corpuscle signalling pathways.
  • ||||||||||  Journal:  Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages. (Pubmed Central) -  Oct 27, 2020   
    Additionally, NiCl-induced apoptosis was dependent on the generation of mtROS, and caspase-1 activation might also partly contribute to the apoptotic process. Altogether, abovementioned results indicate that NiCl induces inflammatory activation in BMDMs via NF-κB, MAPKs, IRF3 signaling pathways as well as NLRP3 inflammasome pathway, which provides a mechanism to improve the efficiency of treatment against Ni-induced allergic reactions.