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Lipopolysaccharide inhibits RELA. 162 / 162
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"Co-incubation with MaR1 (10 nM) significantly attenuated LPS induced NF-kappaB p65 nuclear translocation in BMDMs [nuclear p65 + cells : 16 (3)%, P < 0.01 vs LPS group, XREF_FIG a and b], and partly reduced TNF-alpha levels in the culture medium [494 (49) pg ml -1, P = 0.01 vs LPS group; XREF_FIG c]."
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"These data suggest that HMGB1 and LPS stimulation could downregulate the expression NF-kappaB p65 in cytoplasmic proteins and increase the expression in nuclear proteins, thus leading to modulation of IL-1beta, IL-10, IFN-gamma, and TGF-beta expression; moreover, the suppressive function of Treg cells could be regulated by TLR4."
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"In fact, IkappaB kinase (IKK) assays showed that 1,25 (OH) 2 D 3 attenuated LPS induced IkappaBalpha phosphorylation in macrophages (XREF_FIG), which explains why 1,25 (OH) 2 D 3 stabilized IkappaBalpha protein reported previously, and immunostaining confirmed that 1,25 (OH) 2 D 3 blocked LPS induced p65 nuclear translocation RAW264.7 cells (XREF_FIG)."
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"This treatment pronouncedly alleviated LPS induced neuroinflammatory response, characterized by decreased 5LO, suppressed activation of microglia, decreased NF-kappaB p65, TNF-alpha and IL-1beta, and significantly increased the ratio of p-CREB and CREB or mBDNF and proBDNF in the hippocampus of the LPS challenged mice."
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"We therefore conclude that type I parasites do not inhibit TNF- or LPS stimulated NF-kappaB p65 translocation or TNF stimulated NF-kappaB-mediated transcription, but they may be able to modulate other pathways or host cell transcription factors which are important for expression of a small subset of TNF stimulated genes."
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"Thus, these results indicated that stimulating autophagy can mitigate LPS-induced inflammatory injury in BEECs.Our findings also revealed that overexpression of A20 enhanced autophagy levels, which were hindered by LPS, concomitantly reducing the levels of p-p65 and p-IκBα, preventing p65 from entering the nucleus and ultimately inhibiting NF-κB pathway activation."
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"Unexpectedly, our results revealed that sulfasalazine (SSZ) (a NF-κB inhibitor through inhibition of IκBα degradation) prevented the trans-nucleus of NF-κB p65, but α-M-γ-B did not reverse LPS-induced IκBα degradation and nucleus entry of NF-κB p65 (Fig. 6A and Supporting Information Fig. S5)."
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"In control vector (pcDNA3.0)-treated mice, the LPS challenges (60 and 120 mg/g data were averaged, because the responses were similar) decreased NFkB p50 and p65 protein in the nuclear preparations in lung Intratracheal Plasmid DNA and LPS Lung Injury665Downloaded by [University of Wisconsin - Madison] at 00:54 16 December 2017FIGURE 5 Ribonuclease protection assay showing lung cytokine mRNA profiles after vector pretreatments and LPS challenges."
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"RC intervention in LPS-induced RAW264.7 cells significantly reduced the expression levels of inflammatory factors tumor necrosis factor-α, interleukins-6, iNOS, and CD-86 at the messenger RNA and protein levels, downregulated IκB, p65 protein phosphorylation levels, and significantly inhibited IκB/NF-κB signaling pathway activation."