
IndraLab
Statements
Sulforaphane inhibits NLRP3. 37 / 37
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34
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reach
"A few NLRP3 inflammasome inhibitors, including sulforaphane, isoliquiritigenin, beta-hydroxybutyrate (BHB), flufenamic acid, mefenamic acid, 3,4-methylenedioxy-beta-nitrostyrene (MNS), parthenolide, BAY 11-7082, INF39, and MCC950, have been developed, but there is no evidence showing that these compounds can specifically and directly inhibit NLRP3 itself."
reach
"Different NLRP3 inflammasome inhibitors, including sulforaphane, β-hydroxybutyrate, glyburide, flufenamic acid, mefenamic acid, parthenolide, BAY 11-7082, INF39, and MCC950 have been developed, but there is no evidence demonstrating that these compounds directly and specifically target NLRP3 itself (212)."
sparser
"However, in this area, a number of issues remain to be clarified: (1) What are the exact mechanisms through which 2ccPA and hydroxytyrosol inhibit NLRP3 activation in MS and AD, respectively? (2) What are the molecular mechanisms underlying NLRP3 inhibition by sulforaphane in gout? (3) How do some polyphenols block both canonical and non-canonical NLRP3 assembly? (4) Can phytochemicals targeting both canonical and non-canonical inflammasome activation be regarded as the most reliable pharmacological approaches for the management of CNS, metabolic, and inflammatory diseases? (5) Can a dietary supplementation with phytochemicals prevent or counteract neuroinflammatory and neurodegenerative processes, metabolic alterations, and immune/inflammatory responses? (6) Can phytochemicals exert beneficial effects in CNS, metabolic, and inflammatory diseases through the inhibition of other inflammasomes, including NRLP1, NLRP6, AIM2, and NLRC4?"