IndraLab
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"In this work, we found that glibenclamide could inhibit Nalp3 inflammasomes and Caspase-1 induced by LPS+ high glucose stimulation in cultured peritoneal macrophages, suggesting that the effects of glibenclamide on prevention of serum IL-1beta and TNF-alpha might be related to inhibiting Nalp3 inflammasomes and Caspase-1."
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"The effects of the caspase‐1 inhibitor ZYVAD‐fmk or NLRP3 antagonist glyburide, and treatment with S1P or the S1P receptor regulator FTY720, with or without exposure to cigarette smoke extract were investigated.In alveolar macrophages, cigarette smoke induced increased intracellular expression of IL‐1β (~15%, p<0.05 on pooled data from 3 donors), with particulate staining for cleaved IL‐1β increased both inside and outside the cell (5 fold, p<0.001 on pooled data)."
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"In summary, XREF_FIG provides two important pieces of information : first, that the NLRP3 inflammasome is more active in obese mice, as indicated by a more robust IL-1beta response; and second, that glyburide effectively inhibits the NLRP3 inflammasome, as evidenced by a significant reduction in IL-1beta release."
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"This, in addition to the findings by the same group showing glyburide inhibits the inflammasome upstream of the NLRP3 subunit (likely through inhibition of K ATP channel mediated efflux of K +), provides strong evidence that glyburide is indeed specifically inhibiting NLRP3 inflammasome activation [XREF_BIBR]."
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"Inversely, KD-FANCC increased the expression of p-p38 and NLRP3, which were remarkedly decreased by treatment with BIRB 796 (Additional file 2: Figure S2B–D); however, NLRP3 inhibition by glyburide did not affect p38 phosphorylation, indicating that FANCC regulated NLRP3 expression via a p38-dependent way during inflammation (Fig. 2A–C)."
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"Glombik et al [XREF_BIBR] observed that maternal diabetes causes the activation of NLRP3 inflammasome signaling by increasing the level of the NLRP3 protein subunit, and glyburide, as a NLRP3 inflammasome inhibitor, diminishes the level of NLRP3 protein and caspase-1 subunits, and has particular therapeutic value in anti- metabolic related inflammation."
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"NLRP3 inhibition by glyburide inhibits myocardial contractile dysfunction and decreases myocardial and circulating IL-1β, boosting the survival rate of mice.34 Artemisinin is a traditional Chinese medicine and natural product with significant antimalarial, anti-inflammatory, and immunoregulatory effects.92 Similarly, it decreases mortality rates, serum inflammatory cytokines, adhesion molecule levels, and neutrophil infiltration in the hearts of burn septic mice.65 Artemisinin decreases protein levels of NLRP3/caspase 1 and downregulates mRNA expression of IL-1β and IL-18 in burn sepsis serum-stimulated Raw 264.7 cells."
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"11 A great deal of evidence shows that glibenclamide has anti-inflammatory effect not only in respiratory, but also in digestive, urinary, heart and central nervous system diseases and ischemia-reperfusion injury.44–48 The mechanism of glibenclamide inhibiting NLRP3 activity is still unclear."
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"Glyburide had no effect on NLRP3, caspase-1 and IL-1beta expression as compared with the control group, while the NLRP3, caspase-1 and IL-1beta were decreased by (20.49 +/-7.6)% (t = 2.862, P < 0.01), (32.94 +/-3.44)% (t = 4.154, P < 0.001) and (24.67 +/-5.29)% (t = 2.335, P < 0.05) in the PDGF+ glyburide group, respectively, as compared with the PDGF group."
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"The use of glibenclamide and interference plasmids to inhibit NLRP3 inflammasome activation revealed that the number of CSFV virus gene copies and the virus titer after 24 and 48 h increased following CSFV infection in PBMCs, indicating that NLRP3 had a negative effect on CSFV replication."
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"In our study, we chose glibenclamide not only because of its protective role in neurological diseases by inhibiting K ATP channels, but also because that glibenclamide could abolish the activation of NLRP3 inflammasome in bone marrow derived macrophages (BMDMs) [XREF_BIBR], although the exact mechanism was not fully understood."
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"Finally, specific FDA approved reagents that inhibit molecules involved in asbestos induced inflammation are available : anakinra, an IL-1beta receptor antagonist; infliximab, a chimeric human-mouse anti-TNF-alpha; etanercept, a soluble TNF receptor fusion protein; glyburide, that inhibits the NALP3 inflammasome [XREF_BIBR]."
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"Glibenclamide inhibited NLRP3 inflammasome activation and subsequently protected against organ inflammation and tissue damage either in a cerulean induced obese mouse model of SAP, or in an adenine-diet rat model of chronic kidney disease, or in a cyclophosphamide induced rat model of bladder inflammation, or in a lipopolysaccharide induced myocardial injury in streptozocin induced diabetic rats [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR]."