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  • ||||||||||  Review, Journal:  Functional crosstalk between non-canonical caspase-11 and canonical NLRP3 inflammasomes during infection-mediated inflammation. (Pubmed Central) -  Feb 7, 2020   
    Because the ligands and the mechanisms for the activation of these two inflammasomes are different, studies till date have separately described their roles, although recent studies have reported the functional cooperation between these two inflammasomes during an inflammatory response. This review discusses the studies investigating the functional crosstalk between non-canonical caspase-11 and canonical NLRP3 inflammasomes in the context of inflammatory responses; moreover, it provides insight for the development of novel anti-inflammatory therapeutics to prevent and treat infectious and inflammatory diseases.
  • ||||||||||  Journal:  Ethanol and its metabolites: update on toxicity, benefits, and focus on immunomodulatory effects. (Pubmed Central) -  Feb 7, 2020   
    The section dealing with the beneficial effects of low to moderate alcohol consumption (on cardiovascular system, diabetes, the nervous system and sensory organs, autoimmune diseases, and rheumatology) highlights the importance of anti-inflammatory and immunomodulatory effects in these observations. This knowledge, enriched by a focus on the immunomodulatory effects of ethanol and its metabolites, in particular on the NLRP3 inflammasome pathway, might facilitate the development of treatments that can reduce ethanol's harmful effects or accentuate its beneficial effects.
  • ||||||||||  tacrolimus / Generic mfg.
    Preclinical, Journal:  Tacrolimus reduces atherosclerotic plaque formation in ApoE mice by inhibiting NLRP3 inflammatory corpuscles. (Pubmed Central) -  Feb 6, 2020   
    The protein content of NLRP3, ASC, Casp-1, IL-1β and IL-18 in the aorta in ApoE mice was remarkably increased, and they were inhibited to some extent after tacrolimus intervention. In conclusion, it is speculated that tacrolimus may reduce the formation of AS through inhibiting ROS in macrophages and activation of NLRP3 inflammatory corpuscles and reducing the release of IL-1β and IL-18.
  • ||||||||||  Alverix (amiloride hydrochloride) / Remedica
    Journal:  ENaC-mediated sodium influx exacerbates NLRP3-dependent inflammation in Cystic Fibrosis. (Pubmed Central) -  Feb 1, 2020   
    Overexpression of b-ENaC, in the absence of CFTR dysfunction, increased NLRP3-mediated inflammation, indicating that dysregulated, ENaC-dependent signalling may drive exaggerated inflammatory responses in CF. These data support a role for sodium in modulating NLRP3-inflammasome activation.
  • ||||||||||  AZD1208 / AstraZeneca
    Journal:  Pim-1 as a therapeutic target in human lupus nephritis. (Pubmed Central) -  Jan 31, 2020   
    Chronic stress alone did not exert such effects, but when applied together with high-fructose diet it could partially prevent fructose-induced inflammation, presumably due to increased hepatic glucocorticoids. These data identify Pim-1 as a critical regulator of LN pathogenesis and targeting Pim-1/NFATc1/NLRP3 pathway might be a therapy for human LN.
  • ||||||||||  Azulfidine (sulfasalazine) / Generic mfg.
    Journal, IO Biomarker:  Sulfasalazine as an Immunomodulator of the Inflammatory Process during HIV-1 Infection. (Pubmed Central) -  Jan 31, 2020   
    To be able to demonstrate a clearer genotype-phenotype relationship, all PFS-related genes should be analysed together and the possibility of polygenic inheritance should be considered. Our results suggest that SSZ has an immunomodulatory effect on inflammasome and TLR activation that depends on the clinical HIV status.
  • ||||||||||  Preclinical, Journal, IO Biomarker:  Mechanism of microglia promoting retinal ganglion cell death in vitro (Pubmed Central) -  Jan 30, 2020   
    TLR4-caspase-8-NLRP3 inflammasome pathway is activated in microglia exposed to OGD/R, resulting in the production of IL-1β, thereby contributing to the death of RGCs. (Chin J Ophthalmol, 2020, 56: 32-40).
  • ||||||||||  Preclinical, Journal:  Intermittent Fasting Improves Glucose Tolerance and Promotes Adipose Tissue Remodeling in Male Mice Fed a High Fat Diet. (Pubmed Central) -  Jan 29, 2020   
    IF increased mRNA levels of matrix metallopeptidase 9, which is involved in extracellular matrix degradation, and reduced mRNA levels of collagen 6 alpha-1 and tissue inhibitor of matrix metallopeptidase 1, and fibrosis in gonadal fat in HFD fed mice. In summary, our results show that intermittent fasting improved glucose tolerance in chow and high-fat diet fed mice, and ameliorated adipose tissue inflammation and fibrosis in high-fat diet fed mice.
  • ||||||||||  low molecular weight dextran sulfate (ILB) / TikoMed
    Journal:  L-Fucose ameliorates DSS-induced acute colitis via inhibiting macrophage M1 polarization and inhibiting NLRP3 inflammasome and NF-kB activation. (Pubmed Central) -  Jan 29, 2020   
    We studied the anti-inflammatory effects of L-fucose on Dextran sulfate sodium (DSS)-induced acute colitis in vivo and on LPS/ATP-induced bone marrow derived macrophages (BMDMs) damage in vitro...Finally, L-fucose can inhibit the expression of p-NF-kB in vivo and in vitro. Overall, our results show that L-fucose can attenuate colitis by inhibiting macrophage M1 polarization, inhibiting NLRP3 inflammasome and NF-kB activation, and down-regulation of pro-inflammatory cytokines.
  • ||||||||||  sirolimus / Generic mfg.
    Journal:  The neuroprotection of progesterone against Aβ-induced NLRP3-Caspase-1 inflammasome activation via enhancing autophagy in astrocytes. (Pubmed Central) -  Jan 29, 2020   
    However, pharmacological activation of autophagy by Rapamycin (RAPA) efficiently suppressed Aβ-, lipopolysaccharides (LPS)-induced IL-1β expression via regulating NLRP3-Caspase-1 inflammasome in astrocytes...Taken together, our observations suggest that autophagy-lysosome pathway is one specific molecular mechanism in regulating Aβ-induced NLRP3-Caspase-1 inflammasome activation in astrocytes, particularly uncover the potential neuroprotection of PG in regulating upstream signaling leading to the sequence events of neuroinflammation. That neuroprotective mechanism of PG in regulating NLRP3-Caspase-1 inflammasome can be a potential therapeutic target for ameliorating the pathological procession of AD.
  • ||||||||||  Journal:  Expressions of Thioredoxin Interacting Protein/Nucleotide-binding Oligomerization Domain-like Receptor Protein 3 Inflammasome in the Sciatic Nerve of Streptozotocin-induced Diabetic Rats (Pubmed Central) -  Jan 29, 2020   
    Results The expression of TXNIP protein in the sciatic nerve of diabetic rats was 3.78±0.08,which significantly increased than that in the normal control group(0.99±0.06)(t=26.980,P<0.0001).Compared with the normal control group(0.97±0.05),the expression of NLRP3 protein in the diabetic group(2.44±0.16)was significantly higher(t=8.885,P<0.0001).The expression of cleaved caspase-1 was 4.45±0.19 in the diabetic group and 1.08±0.06 in the normal control group,and the difference was significant(t=16.900,P<0.0001).The expression of IL-1β protein in the diabetic group(4.50±0.16)was significantly higher than that(1.19±0.08)in the normal control group(t=18.630,P<0.0001).Compared with the normal control group,the levels of IL-1β [(110.50±8.80)pg/ml vs.(17.97±3.18)pg/ml,t=9.892,P<0.0001] and IL-18 [(591.70±8.78)pg/ml vs.(160.70±8.33)pg/ml,t=35.620,P<0.0001] in the serum of diabetic rats significantly increased. Conclusion The pathogenesis of diabetic peripheral neuropathy may be related to increased expression of TXNIP,activation of NLRP3 inflammasome,and downstream inflammation,which may provide a new target for diabetic peripheral neuropathy therapy.
  • ||||||||||  Kineret (anakinra) / SOBI, Affibody
    BTK DEFICIENCY LEADS TO NLRP3 INFLAMMASOME DYSREGULATION AND CAUSES MURINE EXPERIMENTAL AND HUMAN IL-1B- MEDIATED COLITIS () -  Jan 28, 2020 - Abstract #DDW2020DDW_2892;    
    Overall, these studies suggest that the activation of BTK in macrophages/dendritic cells serves as a physiologic mechanism of NLRP3 inflammasome regulation in that it blocks the activation of the NLRP3 inflammasome activation. In addition, they provide an explanation for the fact that patients with XLA lacking functional BTK are prone to develop intestinal inflammation which may be amenable to treatment with anti-IL1beta
  • ||||||||||  THE INTERPLAY BETWEEN GUT MICROBIOTA AND NLRP3 ACTIVATION AFFECTS THE SEVERITY OF ACUTE PANCREATITIS IN MICE () -  Jan 28, 2020 - Abstract #DDW2020DDW_2840;    
    With strengthened gut barrier and decreased systematic inflammation, NLRP3 KO mice showed less severe AP as revealed by reduced pancreatic neutrophilic infiltration and necrosis. Conclusion This study identified the activation of NLRP3 by gut microbiota as well as the modulation of gut microbiota by NLRP3 knockout in the progression of AP, which suggest the underlying mechanism of AP-induced gut dysfunction and the critical role of maintaining gut homeostasis in AP recovery.
  • ||||||||||  Composite targeting of nuclear receptors protects mice from NAFLD progression towards HCC (ePoster Area) -  Jan 27, 2020 - Abstract #EASLHCC2020EASL_HCC_236;    
    DCA enhanced expressions of ICAM-I and VCAM-1 partially via direct stimulation on S1PR2 on vascular endothelium, leading to enhanced intestinal lymphocytes migration In conclusion, either INT-767 or antagomiR-21 alone prevent NAFLD progression, with combined targeting more effectively preventing progression towards pre-neoplastic lesions and, ultimately, HCC, thus embodying a putative therapeutic strategy.
  • ||||||||||  Journal:  New insights in neutrophilic asthma. (Pubmed Central) -  Jan 27, 2020   
    This is in stark contrast with the lack of efficacy of different therapies targeting neutrophil chemotaxis and/or signalling cascade, such as IL-17A or CXCR2. Macrolide therapy might be a useful add-on therapy for patients with persistent asthma.
  • ||||||||||  Journal:  Evidence that NLRC4 Inflammasome Mediates Apoptotic and Pyroptotic Microglial Death Following Ischemic Stroke. (Pubmed Central) -  Jan 25, 2020   
    In addition, a functional role for NLRC4 inflammasomes was determined using siRNA knockdown of NLRC4 and pharmacological inhibitors of caspase-1 and -8 to target apoptotic and pyroptotic cell death in BV2 microglial cells under ischemic conditions. In summary, the present study provides evidence that the NLRC4 inflammasome complex mediates the inflammatory response, as well as apoptotic and pyroptotic cell death in microglial cells under in vitro and in vivo ischemic conditions.