IndraLab

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"A study also demonstrated that EGCG blocks both the MyD88-dependent and TRIF-dependent signaling pathways of TLRs in RAW264.7 cells (89)."

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"3) EGCG (20mg/Kg, i.p.), 1, 24 and 48h after paraquat administration in mice, attenuates ALI, the activation of NF-kappaB and upregulation of toll like receptor 2, 4 and 9, as well as their adaptors MyD88 and TRAF6 in the lung."

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"A study also has shown that EGCG inhibits MyD88 dependent signaling pathways and TIR domain containing adaptor inducing IFN-beta (TRIF)-dependent signaling pathways of TLRs in RAW264.7 cells [XREF_BIBR]."

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"EGCG inhibited the activation of NF-κB and the upregulation of TLR 2, 4 and 9 as well as their adaptors MyD88 and TRAF6 in the lungs following PQ challenge."

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"Specifically, EGCG targets and inhibits myeloid differentiation factor 88 (MyD88)- and Toll/interleukin-1 receptor (TIR)-domain-containing adaptor protein inducing interferon beta (TRIF)-dependent signal pathways of TLRs, which are key to the production of inflammatory molecules."

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"In vivo and in vitro studies have demonstrated that EGCG can inhibit the activation of NF-κB and subsequent inflammatory target gene expression via modulation both MyD88- and TRIF-dependent signaling [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In addition, EGCG can finally induce the degradation of TLR-4 co-factor MyD88 adaptor-like (MAL) protein, which links TLR-4 signaling to NF-κB activation, by enhancing the activation of the suppressor of cytokine signaling 1 (SOCS1), which dampens inflammatory responses as a kind of compensatory anti-inflammatory pathway [14] (Figure 5)."