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  • Nepetin limits NLRP3 inflammasome activation and alleviates NLRP3 . . .
    Activation of the NLRP3 inflammasome is associated with the buildup of damaged mitochondria Danger signals released from these impaired mitochondria, such as reactive oxygen species (ROS), oxidize cytosolic mitochondrial DNA (mtDNA), which has been shown to directly stimulate NLRP3 inflammasome activation [8, 9] In contrast, suppressing mitochondrial ROS production and mtDNA has been reported
  • Updated insights into the molecular networks for NLRP3 inflammasome . . .
    A recent study revealed that the heavy chain of ferritin activates the NLRP3 inflammasome in hepatic stellate cells through lysosomal damage , indicating that hepatic fibrogenesis contributes to
  • Inhibition of IRE1α XBP1 axis alleviates LPS-induced acute lung injury . . .
    In this present study, we found that IRE1α-XBP1 axis was activated in LPS-induced mice and Beas-2B cells, and suppressing IRE1α-XBP1 axis can attenuate the acute lung damage, inflammation and cell apoptosis through downregulating TXNIP3 NLRP3 inflammasome activation and ERK p65 signaling pathway (Fig 7) These findings uncovered the role and
  • NLRP3 inflammasome in endothelial dysfunction
    The inflammasome is a molecular platform that drives effector caspase-1 activation, which is assembled by NLRs, AIM2-like receptors (ALRs), or pyrin that can directly or indirectly (via the
  • STAT3 promotes NLRP3 inflammasome activation by mediating NLRP3 . . .
    Recognition of the translocation of NLRP3 to various organelles has provided new insights for understanding how the NLRP3 inflammasome is activated by different stimuli Mitochondria have already
  • Mechanisms of NLRP3 inflammasome-mediated hepatic stellate cell . . .
    Large particulate maters, such as silica and aluminum salt crystals activated the NLRP3 inflammasome via lysosomal damage and rupture 27 This is evidenced by the fact that cathepsin B inhibitor impairs NLRP3 inflammasome activation in human cells 27, 28 Similarly, another study showed that long-term exposure of arsenic (NaAsO 2) resulted in
  • Unraveling the priming phase of NLRP3 inflammasome activation . . .
    As mentioned above, priming signals lead to induction of NLRP3 expression in the late phase This is indispensable for its activation NLRP3 inflammasome activation is inhibited in response to LPS (4 h) and ATP (1 h) in the presence of the new protein synthesis inhibitor cycloheximide [81], [82] NLRP3 expression is dependent on the NF-κB
  • Dynasore Alleviates LPS-Induced Acute Lung Injury by Inhibiting NLRP3 . . .
    Exposure to endotoxin induces macrophages to release tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-12 through transcriptional up-regulation and IL-1β through the activation of the PYD domains-containing protein 3 (NLRP3) inflammasome dynasore was shown to be effective in alleviating macrophage activation in vitro and LPS
  • NLRP3 Inflammasome Activation Through Heart-Brain Interaction Initiates . . .
    The NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3) inflammasome is a cytosolic multiprotein complex that mediates active IL-1β production 10 IL-1β is a proinflammatory cytokine that is critically involved in the pathophysiology of hypertrophic heart disease 4,11 This complex consists of the Nod-like receptor family protein NLRP3, the ASC





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