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  • ||||||||||  Journal:  SAPHO, autophagy, IL-1, FoxO1, and Propionibacterium (Cutibacterium) acnes. (Pubmed Central) -  Dec 2, 2019   
    However, P. acnes itself possibly contributes to FoxO1 down-regulation, like H. pylori infection which induces nuclear inactivation of FoxO1 in human gastric cells to slow down autophagic clearance. As bisphosphonates, which often improve SAPHO syndromes, enhance autophagy, it may be worth testing whether their combination with antibiotics is synergistic in SAPHO syndromes.
  • ||||||||||  Journal:  Neuroepithelial control of mucosal inflammation in acute cystitis. (Pubmed Central) -  Nov 30, 2019   
    Clinical relevance was suggested by elevated urine SP levels in patients with acute cystitis, compared to patients with asymptomatic bacteriuria identifying NK1R/SP as potential therapeutic targets. We propose that NK1R and SP influence the severity of acute cystitis through a neuro-epithelial activation loop that controls pain and mucosal inflammation.
  • ||||||||||  Biomarker, Journal:  NLRP3 inflammasome and lipid metabolism analysis based on UPLC-Q-TOF-MS in gouty nephropathy. (Pubmed Central) -  Nov 29, 2019   
    These data indicated that lipid metabolism and the NLRP3 inflammasome serve a pivotal role in gouty nephropathy. In addition, the results suggested that lipids may mediate the progression of gouty nephropathy through the activity of phospholipase A2, β‑oxidation and activation of the NLRP3 inflammasome.
  • ||||||||||  Review, Journal:  Phytochemicals as Novel Therapeutic Strategies for NLRP3 Inflammasome-Related Neurological, Metabolic, and Inflammatory Diseases. (Pubmed Central) -  Nov 29, 2019   
    The present review article has been intended to provide an integrated and critical overview of the available clinical and experimental evidence about the role of NLRP3 inflammasome in the pathophysiology of neurological, psychiatric, metabolic, and inflammatory diseases, including PD, AD, MS, depression, obesity, type 2 diabetes, arthritis, and intestinal inflammation. Special attention has been paid to highlight and critically discuss current scientific evidence on the effects of phytochemicals on NLRP3 inflammasome pathways and their potential in counteracting central neuroinflammation, metabolic alterations, and immune/inflammatory responses in such diseases.
  • ||||||||||  Kineret (anakinra) / SOBI, Affibody
    Preclinical, Journal:  The inflammasome potentiates influenza/Staphylococcus aureus superinfection in mice. (Pubmed Central) -  Nov 28, 2019   
    A neutrophil elastase inhibitor blocked ASC inflammasome-independent production of IL-1β and the IL-1 receptor antagonist, anakinra, confirmed that IL-1 remains crucial to the clearance of bacteria during superinfection...Collectively, our results demonstrate that ASC augments the clearance of bacteria, but can also contribute to inflammation and mortality. ASC should be considered as a therapeutic target to decrease morbidity and mortality during bacterial superinfection.
  • ||||||||||  Trisenox (arsenic trioxide) / Teva, Medsenic
    Journal:  Taurine attenuates arsenic-induced pyroptosis and nonalcoholic steatohepatitis by inhibiting the autophagic-inflammasomal pathway. (Pubmed Central) -  Nov 28, 2019   
    In mouse livers, we show that arsenic trioxide (AsO) induced NASH, increased autophagy and NLRP3 inflammasome activation, increased lipid accumulation, and resulted in dysregulation of lipid-related genes...These results demonstrated that AsO-induced pyroptosis involves autophagy, CTSB, and the NLRP3 inflammasome cascade, and that Tau alleviates AsO-induced liver inflammation by inhibiting the autophagic-CTSB-NLRP3 inflammasomal pathway rather than decreasing lipid accumulation. These findings give insight into the association of autophagy, inflammation, pyroptosis, and NASH induced by AsO.
  • ||||||||||  Journal:  Involvement of ADAM10 in acrolein-induced astrocytic inflammation. (Pubmed Central) -  Nov 27, 2019   
    Finally, we showed that acrolein induced cell toxicity and decrease of EAAT1 expression, suggesting that acrolein may induce a loss of glutamate uptake function. In conclusion, we demonstrate that acrolein induces astrocytic inflammation through NLRP3 inflammasome, which is regulated by ADAM10 and attributed to p38 MAPK-activated NF-κB p65 activity.
  • ||||||||||  Journal:  Ameliorative effects of echinacoside against spinal cord injury via inhibiting NLRP3 inflammasome signaling pathway. (Pubmed Central) -  Nov 27, 2019   
    In conclusion, we demonstrate that acrolein induces astrocytic inflammation through NLRP3 inflammasome, which is regulated by ADAM10 and attributed to p38 MAPK-activated NF-κB p65 activity. ECH can accelerate motor function recovery in rats following SCI by inhibiting NLRP3 inflammasome-related signaling pathway, suggesting that ECH may serve as a potential therapeutic agent for treating SCI.
  • ||||||||||  Journal:  Expression and Contribution of NLRP3 Inflammasome During the Follicular Development Induced by PMSG. (Pubmed Central) -  Nov 22, 2019   
    Furthermore, a significant increase of ovulation-related genes, hypoxia inducible factor (HIF)-1α and endothelin (ET)-1, was found after 52 h-treatment of PMSG. To our knowledge, it is the first time to clearly indicated the activation of NLRP3 inflammasome may contribute to the ovulation of PMSG-treated ovaries, which will help to further clarify the ovulatory mechanism in mammals.
  • ||||||||||  Journal:  RIPK3-MLKL-mediated necroinflammation contributes to AKI progression to CKD. (Pubmed Central) -  Nov 22, 2019   
    Bone marrow chimeras confirmed that RIPK3-MLKL-dependent necroptosis is responsible for the initiation of the early renal injury after IRI, and then necroptosis triggered NLRP3 inflammasome activation, which subsequently accelerates necroptosis and triggers more inflammation in an auto-amplification loop. These data indicate that necroinflammation driven by RIPK3-MLKL-dependent necroptosis plays a crucial role in the progression of IRI to CKD.
  • ||||||||||  Review, Journal:  P2X7 Receptor Signaling in Stress and Depression. (Pubmed Central) -  Nov 22, 2019   
    Importantly, blockade of P2X7R leads to antidepressant-like effects in different animal models, which corroborates the findings that the gene encoding for the P2X7R is located in a susceptibility locus of relevance to depression in humans. This review will discuss recent findings linked to the P2X7R involvement in stress and MDD neuropathophysiology, with special emphasis on neurochemical, neuroimmune, and neuroplastic mechanisms.
  • ||||||||||  Preclinical, Journal:  Compromised NLRP3 and AIM2 inflammasome function in autoimmune NZB/W F1 mouse macrophages. (Pubmed Central) -  Nov 21, 2019   
    It remains to be established whether the low inflammasome function could contribute to loss of tolerance and the onset of autoimmunity in NZB and NZB/W F1. However, with amplifying inflammatory stimuli through the course of disease, the NLRP3 response in the NZB/W F1 may be sufficient to contribute to kidney damage at later stages of disease.
  • ||||||||||  Journal:  SARS-Coronavirus Open Reading Frame-3a drives multimodal necrotic cell death. (Pubmed Central) -  Nov 21, 2019   
    Finally, SARS 3a activates caspase-1 either directly or via an enhanced potassium efflux, which triggers NLRP3 inflammasome assembly. In summary, Rip3-mediated oligomerization of SARS 3a causes necrotic cell death, lysosomal damage, and caspase-1 activation-all likely contributing to the clinical manifestations of SARS-CoV infection.
  • ||||||||||  Clinical, Journal:  In situ inflammasome activation results in severe damage to the central nervous system in fatal Zika virus microcephaly cases. (Pubmed Central) -  Nov 21, 2019   
    An immunohistochemical analysis of tissues in the neural parenchyma showed significantly higher expression of the receptors NLRP1, NLRP3, and AIM2, cytokines IL-1β, IL-18, and IL-33, and enzymes caspase 1, iNOS, and arginase 1 in ZIKV-positive microcephaly cases than in flavivirus-negative controls. These results suggest that inflammasome activation can aggravate the neuroinflammatory response and consequently increase CNS damage in neonates with fetal neural ZIKV infection and microcephaly.
  • ||||||||||  allopurinol / Generic Mfg.
    Journal, IO Biomarker:  Monosodium Urate Contributes to Retinal Inflammation and Progression of Diabetic Retinopathy. (Pubmed Central) -  Nov 21, 2019   
    These results were associated with effects of the hypouricemic drugs on down-regulating diabetes-induced levels of oxidative stress markers as well as expression of components of the NLRP3 inflammasome such as NLRP3, TLR4 and IL-1β. The outcomes of these studies support a contributing role of MSU in diabetes-induced retinal inflammation and suggest that asymptomatic hyperuricemia should be considered as a risk factor for DR induction and progression.
  • ||||||||||  EFFECT OF NLRP3 INFLAMMASOME IN MRSA INFECTION SECONDARY TO INFLUENZA A VIRUS H1N1 IN VITRO () -  Nov 21, 2019 - Abstract #APSR2019APSR_371;    
    The expression of NLRP3,Caspase-1 mRNA and concentration of IL-1b in supernatant in H1N1+MRSA group were significantly higher than those in blank group (all P<0.01),as well as NLRP3 proteins in immunofluorescence dictation. The expression of IL-1b mRNA was lower in H1N1+MRSA group than that in MRSA group without statistic difference(P=0.21),while the concentration of IL-1b was significantly lower than that in MRSA group(P<0.01).
  • ||||||||||  EFFECT OF NLRP3 INFLAMMASOME IN PNEUMONIA CAUSED BY INFLUENZA A VIRUS H1N1 AND MRSA () -  Nov 21, 2019 - Abstract #APSR2019APSR_366;    
    Histopathological examination showed alveolar interstitial infiltration of inflammatory cells, alveolar septum thickening and oedema in H1N1 group, and more severe in MRSA group. In the H1N1 group, the expression of NLRP3 mRNA and NLRP3 proteins, and the expression of IL-1b mRNA and concentration of IL-1b,all were significantly higher than those in the control group(all P<0.05).The expression of NLRP3 mRNA in MRSA group was higher than that in control group(P=0.03), the difference of NLRP3 proteins between MRSA group and control group wasn't noted.
  • ||||||||||  PM2.5 COULD INDUCE EMT BY NLRP3 INFLAMMASOME ACTIVATION () -  Nov 21, 2019 - Abstract #APSR2019APSR_43;    
    The results shown that IL-1b caused a significant increase of Vimentin and decrease of E-cadherin, which were viewed as two important indicators of the EMT phenomenon. These data revealed that the induction of EMT was involved in the lung cancer risk of PM2.5 in vivo, and IL-1b secreted by NLRP3 inflammasome may involve in EMT to induce the invasion and migration in NSCLC, thereby putatively serving as a novel therapeutic target for PM2.5 induced lung cancer.
  • ||||||||||  Journal:  NLRP3 Inflammasome Activation by MicroRNA-495 Promoter Methylation May Contribute to the Progression of Acute Lung Injury. (Pubmed Central) -  Nov 20, 2019   
    Consistently, elevated miR-495 alleviated lung injury and reduced the neutrophil infiltration and inflammation in rat models of LPS-induced ALI. Taken together, the data in our study demonstrated that methylation of the miR-495 promoter could downregulate miR-495, whose elevation could attenuate the activation of the NLRP3 inflammasome to protect against ALI, which provides novel therapeutic targets for ALI treatment.
  • ||||||||||  Journal:  D-Ribose Induces Podocyte NLRP3 Inflammasome Activation and Glomerular Injury via AGEs/RAGE Pathway. (Pubmed Central) -  Nov 19, 2019   
    Mechanically, AGEs formation inhibition and cleavage or silencing of RAGE gene were shown to suppress D-ribose-induced NLRP3 inflammasome formation and activation, as shown by significant reduction of NLRP3 inflammasome molecular aggregation, caspase-1 activity and IL-1β production. These results strongly suggest that relatively long term administration of D-ribose induces NLRP3 inflammasome formation and activation in podocytes via AGEs/RAGE signaling pathway, which may be one of important triggering mechanisms leading to diabetic nephropathy.
  • ||||||||||  Journal:  Effect of NGR1 on the Atopic Dermatitis Model and its Mechanisms. (Pubmed Central) -  Nov 19, 2019   
    Further, NGR1 treatment inhibited the activation of the NF-κB pathway, and the NLRP3 inflammasome in LPS stimulated RAW264.7 macrophages. The study data indicated that NGR1 might relieve atopic dermatitis via inhibiting inflammation through suppressing the NF-κB signaling pathway and NLRP3 inflammasome activation.