IndraLab

Statements



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"Besides, EGCG down-regulated NF-κB and activated p65 in a dose-dependent manner, and significant difference was shown between untreated control and EGCG treatment groups (100 μM) ( Fig. 4 G)."

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"Epigallocatechin-3-gallate (EGCG), which is the major constituent of green tea, sequestered the p65 subunit of transcription factor nuclear factor-κB in the cytoplasm and inhibited transcriptional activity of the nuclear factor-κB-driven promoter in toll-like receptor-mediated activation, resulting in reduction of inflammatory cytokine production."

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"EGCG also inhibited the upregulation of nuclear factor-kappa B/p65 (NF-kappaB and p65), and induction of cyclooxygenase 2 and inducible nitric oxide synthase."

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"To prove the translocation of NF-κB (p65) prevented by EGCG, we further investigated the changes of protein in the cytoplasm and nuclear by western blotting."

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"Moreover, EGCG inhibited the activation of NF-kappaB and p65, an upstream regulator of COX-2, in A375 melanoma cells, and treatment of cells with caffeic acid phenethyl ester, an inhibitor of NF-kappaB, also inhibited cell migration."

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"EGCG treatment sequesters the p65 subunit of transcription factor NF-kappaB in the cytoplasm and inhibits transcriptional activity of the NF-kappaB-driven promoter in response to CpG-ODN."

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"Treatment with EGCG (20–100 µg/mL) also inhibited cancer cell infiltration and metastasis by downregulating aquaporin 5 (AQP5), NF-κB, and p65 [114]."

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"EGCG pretreatment reversed the activation of NF-κB p65 by LPS as demonstrated by a reduced ratio of phosphorylated p65 to total p65 (p < 0.05)."

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"However, compared to the LPS group, pretreatment with 50 μM EGCG markedly reduced the upregulation of all these genes to levels similar to those of the control group.The binding activity of NF-κB p65 to the IL1B and TNFA promoters was determined using a ChIP–qPCR assay, as shown in Figure 4B."

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"EGCG was found to inhibit the activation of NF-kappaB and p65 in a dose dependent manner."

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"These results suggest that EGCG inhibits oxidative stress and inflammatory responses in the periodontitis model by modulating the Nrf2/HO-1/NLRP3/NF-kappaB p65 signaling pathway, thereby decreasing alveolar bone loss."

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"Taken together, these results suggest that EGCG reduced PCB 126 mediated induction of p65 and suppressed NF-kappaB signaling via preventing PCB 126 induced p65 nuclear translocation in endothelial cells."

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"On the other hand, in future experiments, we could select different animals to induce periodontitis, such as rabbits, to simulate the complex response of the human host to microbial challenge and treatment.In conclusion, this study demonstrated that EGCG (200 mg/kg) inhibited oxidative stress and inflammatory responses in a rat periodontitis model by modulating the Nrf2/HO-1/NLRP3/NF-κB p65 signaling pathway, thereby decreasing alveolar bone loss."

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"In comparison to the glycerol treated group, we observed EGCG at both doses of 5 and 10 mg/kg were able to significantly reduce the immunopositive p65 subunit in the tubular regions of kidney tissues."

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"XREF_BIBR Epigallocatechin-3-gallate (EGCG), a gallic acid ester of catechin, blocks the production of TNF-alpha, IFN-gamma, NF-kB, and p65, which reduces inflammation in the intestinal mucous membrane."

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"EGCG inhibits the activation of NF-kappaB and p65 in a dose dependent manner."

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"Moreover, EGCG inhibited NF-kappaB p65 activity by modulating the cellular localization of p65 and decreasing the transcriptional regulation of NF-kappaB p65 on Twist1 expression."

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"Moreover, EGCG inhibited NF-kappaB p65 activity by modulating the cellular localization of p65 and decreasing the transcriptional regulation of NF-kappaB p65 on Twist1 expression."

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"The TNF-alpha-mediated NF-kappaB (p65) increase in the nuclei was blocked by the treatment of EGCG (XREF_FIG)."

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"Both erlotinib and EGCG or their combination failed to inhibit p65 and Bcl-2 in M4e cells (XREF_FIG)."

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"EGCG alone inhibited NF-kappaBp65 and p-c-Jun (Ser 73) effectively."

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"The combination of EGCG and metformin has been shown to suppress NF-κb, p65, and STAT3 signaling pathways in melanoma cells."