- |||||||||| Preclinical, Journal: LCC18, a benzamide-linked small molecule, ameliorates IgA nephropathy in mice. (Pubmed Central) - Jun 2, 2021
Mechanistic studies show that the mode of action specifically involved: (1) blocking of the MAPKs/COX-2 axis-mediated priming of NLRP3 inflammasome; (2) inhibition of ASC oligomerization and NLRP3 inflammasome assembly by inhibiting NLRP3 binding to PKR, NEK7 and ASC; and (3) activation of autophagy. LCC18 exerts therapeutic effects on murine IgAN by differentially regulating NLRP3 inflammasome activation and autophagy induction, suggesting this new compound as a promising drug candidate to treat IgAN.
- |||||||||| Journal: YAP promotes the activation of NLRP3 inflammasome via blocking K27-linked polyubiquitination of NLRP3. (Pubmed Central) - Jun 2, 2021
Mechanistically, YAP physically interacts with NLRP3 and maintains the stability of NLRP3 through blocking the association between NLRP3 and the E3 ligase β-TrCP1, the latter increases the proteasomal degradation of NLRP3 via K27-linked ubiquitination at lys380. Together, these findings establish a role of YAP in the activation of NLRP3 inflammasome, and provide potential therapeutic target to treat the NLRP3 inflammasome-related diseases.
- |||||||||| Biomarker, Journal: Oxidized mitochondrial DNA released after inflammasome activation is a disease biomarker for myelodysplastic syndromes. (Pubmed Central) - Jun 1, 2021
ox-mtDNA positively and significantly correlated with levels of known alarmins S100A9, S100A8, and apoptosis-associated speck-like protein containing caspase recruitment domain (CARD) specks, which provide an index of medullary pyroptosis. Collectively, these data indicate that quantifiable ox-mtDNA released into the extracellular space upon inflammasome activation serves as a biomarker for MDS and the magnitude of pyroptotic cell death.
- |||||||||| [VIRTUAL] Inflammasome inhibitors for the treatment of muscular dystrophies (Room Paris) - May 30, 2021 - Abstract #EAN2021EAN_991;
MCC950 improved significantly mice performances in vivo, counterbalanced excessive inflammatory and oxidative responses, mitigated necrosis and slowed down the myofibers degradation/regeneration turnover. This molecule could thus offer promising therapeutic prospect for managing DMD or other muscle and inflammatory disorders.
- |||||||||| irbesartan / Generic mfg.
Preclinical, Journal: Effects of irbesartan on myocardial injury in diabetic rats: The role of NLRP3/ASC/Caspase-1 pathway. (Pubmed Central) - May 29, 2021 Compared with DM group, there were no changes in total cholesterol and fasting blood glucose, the degree of myocardial fibrosis cardiac function was attenuated, NLRP3, ASC, Caspase-1 expressions, IL-1β and IL-18 levels were reduced in DM+Ir group. The results suggested that irbesartan may exert myocardial protection by inhibiting the expression of the NLRP3/ASC/Caspase-1 pathway in diabetic rats.
- |||||||||| Clinical, Journal: Clinical Significance of microRNA-146a in Patients with Ulcerative Colitis. (Pubmed Central) - May 29, 2021
From the findings, it is concluded that both melatonin and E2 are efficient to target inflammasome activation in the SCI rats. miRNA-146a was down-regulated in UC patients and was negatively correlated with serum levels of inflammatory factors as well as severity of UC patients.
- |||||||||| dexmedetomidine / Generic mfg.
Preclinical, Journal: Dexmedetomidine inhibits pyroptosis by down-regulating miR-29b in myocardial ischemia reperfusion injury in rats. (Pubmed Central) - May 28, 2021 In conclusion, our studies demonstrate that SSA induces apoptosis and suppresses inflammation in HEKa cells and ameliorates IMQ-induced psoriasis in mice, making it a therapeutic candidate for psoriasis. DEX could ameliorate MIR injury (MIRI) and H/R injury in rats and inhibit H/R induced pyroptosis in myocardial cells via down-regulating miR-29b to activate FoxO3a/ARC axis.
- |||||||||| paracetamol / Generic mfg.
Journal: Baicalin promotes liver regeneration after acetaminophen-induced liver injury by inducing NLRP3 inflammasome activation. (Pubmed Central) - May 28, 2021 Furthermore, the baicalin-provided NLRP3 inflammasome activation and promotion on liver regeneration after APAP-induced liver injury in wild-type mice were diminished in Nrf2 knockout mice. In conclusion, baicalin promoted liver regeneration after APAP-induced acute liver injury in mice via inducing Nrf2 accumulation in cytoplasm that led to NLRP3 inflammasome activation, and then caused the increased expression of IL-18, which induced hepatocytes proliferation.
- |||||||||| Clinical, Journal: Activation of NLRP3 inflammasome assembly is associated with smoking status of patients with coronary artery disease. (Pubmed Central) - May 28, 2021
In conclusion, baicalin promoted liver regeneration after APAP-induced acute liver injury in mice via inducing Nrf2 accumulation in cytoplasm that led to NLRP3 inflammasome activation, and then caused the increased expression of IL-18, which induced hepatocytes proliferation. Our data may imply NLRP3 inflammasome as a mediator of the pro-atherosclerotic property of cigarette smoking in atherosclerotic patients.
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