- |||||||||| Review, Journal: The mechanisms of NLRP3 inflammasome/pyroptosis activation and their role in Parkinson's disease. (Pubmed Central) - May 11, 2019
In this review we focus on the mechanisms of activation of the NLRP3 inflammasome and pyroptosis and their inflammatory effects on the development of PD. In addition, we focus on some inhibitors of NLRP3 inflammatory pathways to alleviate the progression of PD by inhibiting central inflammation and provide new therapeutic strategies for the treatment of PD.
- |||||||||| Preclinical, Journal: Effect of ursolic acid on cardiomyopathy of mice with diabetes and its mechanism (Pubmed Central) - May 11, 2019
In addition, we focus on some inhibitors of NLRP3 inflammatory pathways to alleviate the progression of PD by inhibiting central inflammation and provide new therapeutic strategies for the treatment of PD. Ursolic acid has a obvious protective effect on myocardial injury in mice with diabetes induced by high-fat diet combined with low dose streptozotocin, and its mechanism may be associated with inhibiting NLRP3 inflammasome activation, reducing IL-1β generation and alleviating myocardial inflammatory injury.
- |||||||||| Journal: Total flavonoids in Scutellaria barbata prevents NLRP3 inflammasome expression in tumor cells by affecting autologous pathway (Pubmed Central) - May 9, 2019
Serum IL-1β and IL-18 levels in model control group were found higher than those in control group (P<0.001), but they were significantly lowered in positive control group and TF-SB groups (P<0.05, P<0.01 or P<0.001). Taken together, total flavonoids in S. barbata could effectively alter the tumor growth micro-environment by inhibiting the expression of NLRP3 inflammasome, and its anti-tumor effect may be associated with the induction of tumor cell autophagy.
- |||||||||| Review, Journal: Emerging role of the P2X7-NLRP3-IL1β pathway in mood disorders. (Pubmed Central) - May 9, 2019
We present, in the way of reviewing relevant literature, the preclinical data and scientific rationale supporting the role of the P2X7-NLRP3-IL-1β pathway in mood disorders. We also highlight recent advances in drug discovery and development of P2X7 small molecule antagonists and P2X7 PET ligands which provide optimism that clinical tools are availableto address critical proof-of-concept experiments in mood disorders.
- |||||||||| Journal: Associations of variants In the hexokinase 1 and interleukin 18 receptor regions with oxyhemoglobin saturation during sleep. (Pubmed Central) - May 9, 2019
Four additional significant regions were detected in secondary sex-stratified and combined discovery and replication analyses, including a region overlapping Reelin, a known marker of respiratory complex neurons.These are the first genome-wide significant findings reported for oxyhemoglobin saturation during sleep, a phenotype of high clinical interest. Our replicated associations with HK1 and IL18R1 suggest that variants in inflammatory pathways, such as the biologically-plausible NLRP3 inflammasome, may contribute to nocturnal hypoxemia.
- |||||||||| Journal, IO Biomarker: Inhibition of Caspase-1-dependent pyroptosis attenuates copper-induced apoptosis in chicken hepatocytes. (Pubmed Central) - May 8, 2019
Furthermore, treatment with Cu and Z-YVAD-FMK could down-regulate the mRNA levels of Caspase-3, Bak1, Bax, and CytC and Caspase-3 protein expression, up-regulate the mRNA expression of Bcl2, increase the MMP and reduce cell apoptosis compared to treatment with Cu in hepatocytes. Collectively, these finding evidenced that excess Cu induced pyroptosis by generating ROS in hepatocytes, and the inhibition of Caspase-1-dependent pyroptosis might attenuate Cu-induced apoptosis.
- |||||||||| Preclinical, Journal: NLRP3 deficiency ameliorates renal inflammation and fibrosis in diabetic mice. (Pubmed Central) - May 7, 2019
Furthermore, we also found exposure of IL-1β to HK-2 cells induced ROS generation and expression of TXNIP and Nox4. Taken together, inhibition of NLRP3 inflammasome activation inhibits renal inflammation and fibrosis at least in part via suppression of oxidative stress in diabetic nephropathy.
- |||||||||| Biomarker, Journal: NEOPTERIN PRECONDITIONING PREVENTS INFLAMMASOME ACTIVATION IN MAMMALIAN ASTROCYTES. (Pubmed Central) - May 7, 2019
Mechanistically, neopterin might induce eletrophilic stress and consequently the nuclear translocation of the transcription factor Nrf-2, and the anti-inflammatory cytokines IL-10 and IL-1ra release, which would induce the inhibition of the inflammasome activation. Altogether, this strongly suggests an essential role of neopterin during inflammatory processes.
- |||||||||| Journal: Suppression of miR-21 and miR-155 of macrophage by cinnamaldehyde ameliorates ulcerative colitis. (Pubmed Central) - May 7, 2019
Meanwhile, data revealed that transferred miR-21 or miR-155 inhibitor suppressed levels of IL-1β and IL-6, whereas miR-21 or miR-155 mimics increased expressions of these, and CA suppressed these expressions. Our results indicate that CA could ameliorate DSS-induced colitis through inhibition of NLRP3 inflammasome activation and miR-21 and miR-155 levels in colons and macrophage, suggesting that CA might be a potentially effective drug for UC.
- |||||||||| praziquantel (MSC2499550A) / Merck (MSD)
Journal: The use of gold nanorods as a new vaccine platform against schistosomiasis. (Pubmed Central) - May 5, 2019 ...At present, the main strategy adopted for the control of schistosomiasis is the use of safe chemotherapy, such as praziquantel...Furthermore, AuNRs-NH-rSm29 could activate dendritic cells in vitro, enhancing MHCII and MHCI expression and the production of IL-1β in a NLRP3-, ASC- and Caspase-1-dependent manner. In summary, our findings support the use of nanorods as an immunization strategy in vaccine development against infectious diseases.
- |||||||||| sirolimus / generics
Journal: Acrolein induces NLRP3 inflammasome-mediated pyroptosis and suppresses migration via ROS-dependent autophagy in vascular endothelial cells. (Pubmed Central) - May 2, 2019 ...In our study, 3-methyladenine (3-MA), an autophagy inhibitor, aggravated NLRP3 inflammasome activation, pyroptosis and decreased cell migration, rapamycin (Rapa), an autophagy inducer, alleviated aforementioned phenomenon under acrolein stress...In conclusion, it is possible that acrolein induced cell pyroptosis and suppressed cell migration via ROS-dependent autophagy. What's more, NLRP3 inflammasome activation plays a key role in this process.
- |||||||||| Review, Journal: The role of mitochondria in NLRP3 inflammasome activation. (Pubmed Central) - May 2, 2019
These molecules bind to NLRP3 that is translocated on mitochondria and activate the NLRP3 inflammasome. Here we review recently described mechanisms by which mitochondria regulate NLRP3 inflammasome activation.
- |||||||||| Journal: A comparative analysis of the capacity of the Candida species to elicit vaginal immunopathology. (Pubmed Central) - May 2, 2019
Collectively, our findings demonstrate that although NAC species are increasingly reported as causative agents of VVC, C. albicans appears to be exceedingly vaginopathogenic, exhibiting robust immunopathology, hypha formation and Candidalysin expression. Thus, this study provides mechanistic insight as to why C. albicans is overwhelmingly the major pathogen reported during VVC.
- |||||||||| Journal: Increased gene copy number of DEFA1/DEFA3 worsens sepsis by inducing endothelial pyroptosis. (Pubmed Central) - May 2, 2019
Based on these findings, we engineered a monoclonal antibody against HNP-1 to block the interaction with P2X7 and found that the blocking antibody protected mice carrying high copy number of DEFA1/DEFA3 from lethal sepsis. We thus demonstrate that DEFA1/DEFA3 copy number variation strongly modulates sepsis development in vivo and explore a paradigm for the precision treatment of sepsis tailored by individual genetic information.
- |||||||||| low molecular weight dextran sulfate (ILB) / TikoMed
Journal: Curcumin alleviates DSS-induced colitis via inhibiting NLRP3 inflammsome activation and IL-1β production. (Pubmed Central) - May 1, 2019 We thus demonstrate that DEFA1/DEFA3 copy number variation strongly modulates sepsis development in vivo and explore a paradigm for the precision treatment of sepsis tailored by individual genetic information. Curcumin could strongly suppress DSS-induced NLRP3 inflammsome activation and alleviate DSS-induced colitis in mice, thus it may be a promising candidate drug in clinical application for IBD therapy.
- |||||||||| Journal: The role of Nrf2 in NLRP3 inflammasome activation. (Pubmed Central) - May 1, 2019
It was revealed that the impact caused by COFs-derived PM on blood vessel formation through a ROS-mediated NLRP3 inflammasome pathway. No abstract available
- |||||||||| Clinical, Review, Journal: A Guide to IL-1 family cytokines in adjuvanticity. (Pubmed Central) - Apr 30, 2019
The coordinated release of IL-1 family members in response to adjuvant-induced damage or cell death may be a determining factor in the transition from local inflammation to the induction of an adaptive response. Here, we analyse the effects of IL-1 family cytokines on innate and adaptive immunity with a particular emphasis on activation of antigen presenting cells and induction of T cell-mediated immunity, and we address in detail the contribution of these cytokines to the modes of action of vaccine adjuvants including those currently approved for human use.
- |||||||||| Journal: Association of Type 2 Diabetes with Submicron Titanium Dioxide Crystals in the Pancreas. (Pubmed Central) - Apr 30, 2019
In this pilot study of 11 pancreatic specimens, 8 of the type 2 diabetic pancreas and 3 of the non-diabetic pancreas, we show that 110±70 nm average diameter TiO2 crystals abound in the type 2 diabetic pancreas, but not in the non-diabetic pancreas. In the type 2 diabetic pancreas, their count is as high as 108 -109 per gram.
- |||||||||| Journal: Coenzyme Q10 serves to couple mitochondrial oxidative phosphorylation and fatty acid β-oxidation, and attenuates NLRP3 inflammasome activation. (Pubmed Central) - Apr 30, 2019
In contrast, supplementation with CoQ10 significantly recovered mitochondrial function and concurrently decreased the generation of reactive oxygen species and lipid peroxides, inhibited the accumulation of lipid droplets and the formation of the NOD-like receptor family pyrin domain-containing three (NLRP3) inflammasome, and reduced interleukin-1β release and cell death. These results clarify the causal role of CoQ10 in coupling the electron transport chain with β-oxidation, which may promote the development of CoQ10-directed therapies for MADD patients.
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