The NLRP3 inflammasome is a multi-protein complex that initiates innate immunity responses when exposed to a wide range of stimuli, including pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs). Inflammasome activation leads to the release of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 and to pyroptotic cell death. Over-activation of NLRP3 inflammasome has been associated with several chronic inflammatory diseases. A deep knowledge of NLRP3 inflammasome biology is required to better exploit its potential as therapeutic target and for the development of new selective drugs. To this purpose, in the past few years, several tools have been developed for the biological characterization of the multimeric inflammasome complex, the identification of the upstream signaling cascade leading to inflammasome activation, and the downstream effects triggered by NLRP3 activation. In this review, we will report cellular models and cellular, biochemical, and biophysical assays that are currently available for studying inflammasome biology. A special focus will be on those models/assays that have been used to identify NLRP3 inhibitors and their mechanism of action.
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http://dx.doi.org/10.3390/ijms21124294 | DOI Listing |
Adv Sci (Weinh)
January 2025
State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, College of Veterinary Medicine, Jilin University, Changchun, Jilin, 130062, China.
Staphylococcus aureus (S. aureus) is a major zoonotic pathogen, with mammary gland infections contributing to mastitis, a condition that poses significant health risks to lactating women and adversely affects the dairy industry. Therefore, understanding the immune mechanisms underlying mammary infections caused by S.
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January 2025
Department of Eye Center, Xiangya Hospital, Central South University, Changsha, China.
Fatty acid binding proteins (FABPs) are a class of small molecular mass intracellular lipid chaperone proteins that bind to hydrophobic ligands, such as long-chain fatty acids. FABP5 expression was significantly upregulated in the N-methyl-d-aspartic acid (NMDA) model, the microbead-induced chronic glaucoma model, and the DBA/2J mice. Previous studies have demonstrated that FABP5 can mediate mitochondrial dysfunction and oxidative stress in ischemic neurons, but the role of FABP5 in oxidative stress and cell death in retina NMDA injury models is unclear.
View Article and Find Full Text PDFPhytother Res
January 2025
Laboratory of Molecular NeuroTherapeutics, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Raebareli, Uttar Pradesh, India.
Background And Aim: Hepatic encephalopathy (HE) is a complex neurological disorder in individuals with liver diseases, necessitating effective neuroprotective interventions to alleviate its adverse outcomes. Berberine (BBR), a natural compound with well-established anti-fibrotic and neuroprotective properties, has not been extensively studied in the context of glial activation under hyperammonaemic conditions. This study evaluates the neuroprotective potential of BBR in a thioacetamide (TAA)-induced HE rat model, focusing on its effects on glial activation and NLRP3 inflammasome signalling.
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January 2025
Third Department of Obstetrics and Gynecology, University General Hospital "ATTIKON", Medical School, National and Kapodistrian University of Athens, 12462 Athens, Greece.
Chronic inflammation is increasingly recognized as a critical factor in female reproductive health; influencing natural conception and the outcomes of assisted reproductive technologies such as in vitro fertilization (IVF). An essential component of innate immunity, the NLR family pyrin domain-containing 3 (NLRP3) inflammasome is one of the major mediators of inflammatory responses, and its activation is closely linked to oxidative stress. This interaction contributes to a decline in oocyte quality, reduced fertilization potential, and impaired embryo development.
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January 2025
Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK.
Sandhoff disease (SD) is a progressive neurodegenerative lysosomal storage disorder characterized by GM2 ganglioside accumulation as a result of mutations in the gene, which encodes the β-subunit of the enzyme β-hexosaminidase. Lysosomal storage of GM2 triggers inflammation in the CNS and periphery. The NLRP3 inflammasome is an important coordinator of pro-inflammatory responses, and we have investigated its regulation in murine SD.
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