- |||||||||| Journal, Myeloid-derived suppressor cells: Ablation of NLRP3 inflammasome rewires MDSC function and promotes tumor regression. (Pubmed Central) - Aug 30, 2022
Finally, therapeutic targeting of NLRP3 inhibited tumor development and re-programmed the MDSC compartment. These findings propose that targeting NLRP3 in MDSCs could overcome tumor-induced tolerance and may provide new checkpoints of cancer immunotherapy.
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Our findings suggest that TMEM16F participates in neuroinflammation in Alzheimer's disease through participating in polarization of microglia and activation of the NLRP3 inflammasome. These results indicate that TMEM16F inhibition may be a potential therapeutic approach for Alzheimer's disease treatment.
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Besides, propofol may reduce p-Tau accumulation by modulating SOD and HO-1 expression through p62/Keap1/Nrf2 pathway. Interference with miRNA-155 can inhibit the NLRP3 pathway of MDA-MB-231 cells, as well as the proliferation, migration and inflammatory factor secretion of MDA-MB-231 cell, and can accelerate its apoptosis.
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Preclinical, Journal: miR-155-5p/FOXO3a promotes pulmonary fibrosis in rats by mediating NLRP3 inflammasome activation. (Pubmed Central) - Aug 24, 2022 Bleomycin-induced PF rat model was established...miR-155-5p inhibition and silencing FOXO3a exacerbated alveolitis and PF in rats and increased levels of NPRP3, ASC, caspase-1, IL-1β, and IL-18. miR-155-5p aggravated alveolitis and promoted PF by targeting FOXO3a and prompting the activation of NLRP3 inflammasome and then inducing IL-1β and IL-18 release.
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gp78 or Insig-1 deficiency in myeloid cells led to exacerbated NLRP3 inflammasome-dependent inflammation in vivo, including lipopolysaccharide-induced systemic inflammation and alum-induced peritonitis. Taken together, our study identifies gp78-mediated NLRP3 ubiquitination as a regulatory mechanism that restrains inflammasome activation and highlights NLRP3 ubiquitination as a potential therapeutic target for inflammatory diseases.
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Journal: Sapidolide A alleviates acetaminophen-induced acute liver injury by inhibiting NLRP3 inflammasome activation in macrophages. (Pubmed Central) - Aug 5, 2022 The in vivo assessments conducted on mice pretreated with SA (25, 50 mg/kg, ip) then with a single dose of APAP (400 mg/kg, ip) showed that SA significantly alleviated inflammatory responses of AILI by inhibiting the expression and activation of the NLRP3 inflammasome. In general, the results reported herein revealed that SA exerts anti-inflammatory effects by regulating NLRP3 inflammasome activation in macrophages, which suggests that SA has great a potential for use in the treatment of AILI patients.
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