NLRP3 inhib 
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  • ||||||||||  Preclinical, Journal, IO Biomarker:  Role of microglial activation and neuroinflammation in neurotoxicity of acrylamide in vivo and in vitro. (Pubmed Central) -  Jul 4, 2020   
    In vitro studies using BV-2 microglial cells confirmed microglial inflammatory response, as evident by time- (0-36 h; 50 μM) and dose- (0-500 μM; 24 h) dependent increase in mRNA expression of IL-1β and IL-18, as well as the inflammatory marker iNOS. Furthermore, acrylamide-induced upregulation of pro-inflammatory cytokines was mediated through the NLRP3 inflammasome pathway, as evident by increased expression of NLRP3, caspase 1, and ASC in the rat cerebral cortex, and by the inhibitory effects of NLRP3 inflammasome inhibitor on the acrylamide-induced upregulation of NLRP3, caspase 1, IL-1β, and IL-18 in BV-2 microglia.
  • ||||||||||  Preclinical, Journal:  ATP induces caspase-3/gasdermin E-mediated pyroptosis in NLRP3 pathway-blocked murine macrophages. (Pubmed Central) -  Jul 4, 2020   
    In RAW264.7 cells, knockdown of GSDME by small interfering RNA attenuated ATP-induced lytic cell death and HMGB1 release into culture supernatants. Collectively, our results indicate that ATP induces pyroptosis in macrophages through the caspase-3/GSDME axis when the canonical NLRP3 pathway is blocked, suggestive of an alternative mechanism for combating against pathogen evasion.
  • ||||||||||  Journal, IO Biomarker:  Serum amyloid A-mediated inflammasome activation of microglial cells in cerebral ischemia. (Pubmed Central) -  Jul 4, 2020   
    These studies suggest that brain injury to can elicit a systemic inflammatory response mediated through SAA that contributes to the pathological outcomes.SIGNIFICANCE STATEMENTIn the present study, SAA can induce that activation of the inflammasome in microglial cells and give rise to IL-1β release which can further inflammation in the brain following neurological diseases. The also presents a novel target for therapeutic approaches in stroke.
  • ||||||||||  Clinical, Clinical data, Review, Journal, Adverse events:  Obesity and COVID-19: Immune and metabolic derangement as a possible link to adverse clinical outcomes. (Pubmed Central) -  Jul 3, 2020   
    Endothelial dysfunction and arterial stiffness could favor the recently discovered infection of the endothelium by SARS-CoV-2, while alterations in cardiac structure and function and the pro-thrombotic microenvironment in obesity could provide a link for the increased cardiovascular events in these patients. The successful use of anti-inflammatory agents such as IL-1 and IL-6 blockers in similar hyper-inflammatory settings like that of rheumatoid arthritis has triggered the discussion of whether such agents could be administrated in selected patients with COVID-19 disease.
  • ||||||||||  Preclinical, Journal:  Sex-Specific Effects of the Nlrp3 Inflammasome on Atherogenesis in LDL Receptor-Deficient Mice. (Pubmed Central) -  Jul 3, 2020   
    Thus, castration increased the dependency of atherosclerosis on the NLRP3 inflammasome, suggesting that testosterone may block inflammation in atherogenesis. Conversely, ovariectomy reduced the dependency on NLRP3 inflammasome components for atherogenesis, suggesting that estrogen may promote inflammasome-mediated atherosclerosis.
  • ||||||||||  Review, Journal:  Mechanisms of Cardiovascular Benefits of Sodium Glucose Co-Transporter 2 (SGLT2) Inhibitors: A State-of-the-Art Review. (Pubmed Central) -  Jul 3, 2020   
    Several potential theses have been proposed to explain the cardioprotective effects of SGLT2 inhibition, which include diuresis/natriuresis, blood pressure reduction, erythropoiesis, improved cardiac energy metabolism, inflammation reduction, inhibition of the sympathetic nervous system, prevention of adverse cardiac remodeling, prevention of ischemia/reperfusion injury, inhibition of the Na/H-exchanger, inhibition of SGLT1, reduction in hyperuricemia, increasing autophagy and lysosomal degradation, decreasing epicardial fat mass, increasing erythropoietin levels, increasing circulating pro-vascular progenitor cells, decreasing oxidative stress, and improving vascular function. The strengths and weaknesses of these proposed mechanisms are reviewed in an effort to try to synthesize and prioritize the mechanisms as they relate to clinical event reduction.
  • ||||||||||  Journal:  Taking Sex Seriously: An Oft-Overlooked Biological Variable. (Pubmed Central) -  Jul 3, 2020   
    The strengths and weaknesses of these proposed mechanisms are reviewed in an effort to try to synthesize and prioritize the mechanisms as they relate to clinical event reduction. No abstract available
  • ||||||||||  Journal:  Regulatory T cells in paracoccidioidomycosis. (Pubmed Central) -  Jul 2, 2020   
    It is demonstrated that some of these components are involved in the negative control of Treg cell expansion, whereas others positively trigger the proliferation and activity of these cells. Finally, the studies here summarized highlight the dual role of Treg cells in PCM, which can be protective by controlling excessive immunity and tissue pathology but also deleterious by inhibiting the anti-fungal immunity necessary to control fungal growth and dissemination.
  • ||||||||||  Journal:  Inflammasomes, Neutrophil Extracellular Traps, and Cholesterol. (Pubmed Central) -  Jul 2, 2020   
    In humans, inflammasome activation and NETosis may contribute to atherosclerotic plaque erosion and thrombosis, especially in patients with type 2 diabetes, chronic kidney disease, or clonal hematopoiesis. Suppression of the inflammasome by activation of cholesterol efflux or by direct inhibition of inflammasome components may benefit patients with cardiovascular disease and underlying susceptibility to inflammasome activation.
  • ||||||||||  eplerenone / Generic mfg.
    Preclinical, Journal:  Eplerenone Ameliorates Cell Pyroptosis in Contralateral Kidneys of Rats with Unilateral Ureteral Obstruction. (Pubmed Central) -  Jul 2, 2020   
    Suppression of the inflammasome by activation of cholesterol efflux or by direct inhibition of inflammasome components may benefit patients with cardiovascular disease and underlying susceptibility to inflammasome activation. Our data suggest that the activation of MR is involved in NLRP3/caspase-1 pathway-induced cell pyroptosis in the contralateral kidney of UUO model.
  • ||||||||||  [VIRTUAL] Glucagon induces the hepatic expression of acute-phase proteins and pro-inflammatory cytokines (Poster Hall) -  Jul 2, 2020 - Abstract #EASD2020EASD_437;    
    Identification of these pathways and cellular processes contributes to a better understanding of RVVC and may open new therapeutic avenues. These results suggest that glucagon has pro-inflammatory effects that may help to elucidate the mechanism by which glucagon contributes to hyperglycemia in addition to the well known stimulatory effect on hepatic gluconeogenesis.
  • ||||||||||  Cytovene (ganciclovir) / Roche, irinotecan / Generic mfg.
    Journal, IO Biomarker:  Ganciclovir reduces irinotecan-induced intestinal toxicity by inhibiting NLRP3 activation. (Pubmed Central) -  Jul 2, 2020   
    Furthermore, GCV + irinotecan did not decrease the anti-tumor effect of irinotecan in vivo. In summary, GCV had intestine-protective and anti-inflammatory properties that possibly reduced irinotecan-induced intestinal dysfunction.
  • ||||||||||  Review, Journal:  NLRP3 Inflammasome Signaling as a Link Between HIV-1 Infection and Atherosclerotic Cardiovascular Disease. (Pubmed Central) -  Jul 1, 2020   
    Here we describe the pro-inflammatory state of HIV-1 infection that leads to increased risk of cardiovascular disease, the role of the NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome in HIV-1 infection, the role of the NLRP3 inflammasome in cardiovascular disease (CVD), and outline a model whereby HIV-1 infection can lead to atherosclerotic disease through NLRP3 inflammasome activation. Our discussion highlights the literature supporting HIV-1 infection as a stimulator of the NLRP3 inflammasome as a driver of atherosclerosis.
  • ||||||||||  tamoxifen / Generic mfg.
    [VIRTUAL] Anti-tumor effects and mechanism of 4′-bromo-resveratrol in a BRAFV600E/ PTENNULL melanoma mouse model () -  Jul 1, 2020 - Abstract #SID2020SID_573;    
    Tumors were induced by topical application of 4-hydroxytamoxifen on shaved backs of 10-week-old mice, and the effects of 4-BR (30 mg/kg b.wt.; intraperitoneally; 3d/week for 5 weeks) treatment were assessed on pigmented melanoma tumors...Results indicated that 4BR significantly downregulated (≥2-fold) expression of multiple genes promoting melanoma metastasis (Fn1, S1008a, Fap, Col3a1, Angpt2, Itga1, and Ptgs2), associated with chemokine/cytokines and their receptors (Ccr1, Ccl6, Il1b, Ccl24, Ccl9, Il1rl1 and Ccr5), and innate/adaptive immunity (Itgam, Nlrp3, Colec12 and Irf7). Overall, sirtuin inhibition by 4BR (or other means) appears to be a promising anti-cancer therapy with anti-metastatic and immunomodulatory effects, warranting further studies, including clinical investigations.
  • ||||||||||  Journal:  Influenza Virus-Induced Oxidized DNA Activates Inflammasomes. (Pubmed Central) -  Jun 30, 2020   
    In addition, we show that influenza virus stimulates IL-1β secretion from macrophages in an AIM2-dependent manner. These results provide a missing link between influenza viral proteins and the NLRP3 inflammasome activation and reveal the importance of influenza virus-induced oxidized DNA in inflammasomes activation.
  • ||||||||||  sirolimus / Generic mfg.
    Journal:  Rapamycin improves the neuroprotection effect of inhibition of NLRP3 inflammasome activation after TBI. (Pubmed Central) -  Jun 29, 2020   
    Collectively, the data demonstrate that mitophagy and NLRP3 inflammasome have the interactivity, and Rap-induced mitophagy further enhances the neuroprotection of inhibition of NLRP3 inflammasome activation post-TBI. Our findings suggest that Rap-activated mitophagy combined with MCC950-induced NLRP3 inflammasome repression may be a potential strategy for TBI therapy.
  • ||||||||||  cyclosporine / Generic mfg.
    Journal:  Impaired mitophagy triggers NLRP3 inflammasome activation during the progression from nonalcoholic fatty liver to nonalcoholic steatohepatitis. (Pubmed Central) -  Jun 29, 2020   
    The addition of cyclosporine A did not change LC3II/Τοmm20 ratios; but P62 levels were increased after an extended duration of PA exposure, indicating a defect in autophagic activity...The findings suggest that impaired mitophagy triggers hepatic NLRP3 inflammasome activation in a murine NASH model and primary hepatocytes. The new insights into inflammasome activation through mitophagy advance our understanding of how fatty acids elicit lipotoxicity through oxidant stress and autophagy in mitochondria.
  • ||||||||||  Journal:  3D chitosan scaffolds impair NLRP3 inflammasome response in macrophages. (Pubmed Central) -  Jun 29, 2020   
    Interestingly, our results are in contrast with studies reported in the literature that indicate that chitosan is a powerful activator of the NLRP3 inflammasome in nanoscale chitosan products. Our studies that were performed in large scale chitosan scaffolds, stress out that the process of phagocytosis is pivotal in inflammasome assembly and activation, are rather important since they clearly illustrate the different role of the inflammasome in the biological response to large scale and nanoscale biomaterials.
  • ||||||||||  Journal:  Dectin-2-induced CCL2 production in tissue-resident macrophages ignites cardiac arteritis. (Pubmed Central) -  Jun 29, 2020   
    IL-1β then activated cardiac endothelial cells to express CXCL1 and CCL2 and adhesion molecules that induced neutrophil and further iMo recruitment and accumulation in the aortic root and coronary arteries. Our findings demonstrate that Dectin-2-mediated induction of CCL2 production by macrophages resident in the aortic root and coronary arteries initiates vascular inflammation in a model of Kawasaki disease, suggesting an important role for the innate immune system in initiating vasculitis.
  • ||||||||||  Journal:  The NLRP3 inflammasome as pharmacological target. (Pubmed Central) -  Jun 29, 2020   
    Thus, compounds that prevent NLRP3 inflammasome activation are of common interest with relevant therapeutic potential. The focus of this review is recent developments in NLRP3 inflammasome inhibitors.
  • ||||||||||  Journal:  NLRP3 inflammasome in cardioprotective signaling. (Pubmed Central) -  Jun 29, 2020   
    Therefore, in this review we focus on beneficial, cardioprotective properties of the NLRP3 inflammasome and its components NLRP3, ASC and caspase-1. The results show that 1) NLRP3 deficiency prevents cardioprotection in isolated heart by ischemic preconditioning and in vivo heart by TLR2 activation, associated with impaired STAT3 or Akt signaling, respectively; 2) ASC deficiency also prevents in vivo TLR2-mediated protection; and 3) caspase-1 inhibition results in decreased infarction but impaired protection through the Akt pathway during mild ischemic insults.In conclusion, the NLRP3 inflammasome is not only detrimental, it can also be involved in cardioprotective signaling, thus fueling the future challenge to acquire a full understanding of NLRP3 inflammasome role in cardiac IR before embarking on clinical trials using NLRP3 inhibitors.