IndraLab
Statements
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"The present data indicated that emodin inhibited TLR4 signaling via both MyD88-dependent and -independent pathways, and thus it was hypothesized that the antitumor activity of emodin depends on the inhibition of NF-κB via downregulation of the TLR4 signaling pathway.The present study revealed downregulation of proliferative factors, including c-Myc, cyclin D1 and PCNA, as well downregulation of anti-apoptotic Bcl-2, and upregulation of the pro-apoptotic factor Bax in PTC cell lines exposed to emodin."
reach
"Therefore, we determined the expression levels of these related proteins, and the results indicated that emodin could significantly downregulate the HTRA1, IL-33, MyD88, TRAF-6, and NF-kappaB protein levels, but upregulate the TGF-beta1 protein level, and decrease the TNF-alpha, IL-1beta, and IL-6 mRNA levels."