IndraLab

Statements



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"The ROS inducing effects and the NF-kappaB inhibitory effects decreased the activity of the nuclear p65, affected cell cycle progression, and induced cell death in cancer cells."

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"In vivo and in vitro studies were used to investigate whether PEG-CeNP treatment modulated microglial polarization via inhibiting ROS induced NF-kappaB p65 translocation."

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"We found that TNF-alpha-induced NF-kappaB and RelA Ser (276) phosphorylation, a modification critical for its transcriptional activity, was inhibited by abrogation of the ROS signaling pathway, whereas NF-kappaB and RelA Ser (536) phosphorylation was not."

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"In addition, physalin F abrogated the nuclear translocation of p65 and p50 subunits that were reversed by both ROS scavengers, NAC and GSH (XREF_FIG)."

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"Thus, these analogs exert antiproliferative effects through two independent mechanisms of action, acting both as ROS inducing agents and NF-kappaB p65 inhibition in TNBC cells."

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"In our study, NAC pretreatment improved total and phospho-NF-kappaB p65 and RelA expression, indicating that excessive ROS inhibited p65 and RelA production directly."

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"PEG-CeNP treatment modulated microglial polarization via inhibiting ROS induced NF-kappaB p65 translocation."

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"Reactive oxygen species (ROS) depletion and neutralization of p65 subunit of NF-κB in LPS-treated neutrophils decreased TLR10 expression."

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"In addition, inhibition of ROS by NAC also suppressed MCM triggered LC3 II accumulation and degradation of NF-kappaBp65, a cargo of autophagosomes in MCM polarized macrophages 5, or p62."

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"PEG-CeNP treatment hindered A1 astrocyte alteration via inhibiting ROS induced NF-kappaB p65 translocation."

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"In vitro, NF-kappaB p65 and GFAP immunostaining and western blotting were performed to investigate whether PEG-CeNP treatment inhibited A1 astrocyte via inhibiting ROS induced NF-kappaB p65 translocation."

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"In line with these reports, our results have revealed that PGE treatment contributed to the improvement in hyperlipidemia as a result of a reduction in ROS mediated p65 induction of miR-145 expression in alloxan-diabetic rats."

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"In our study, NAC pretreatment improved total and phospho-NF-kappaB p65 and RelA expression, indicating that excessive ROS inhibited p65 and RelA production directly."

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"These results partly support our conjecture that PEG-CeNP treatment promoted remyelination via inhibiting ROS induced NF-kappaB p65 translocation and modulating skewed microglia polarization."