IndraLab

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NAC inhibits JUN. 7 / 7
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"This work investigated the capacity of alpha-lipoic acid (LA) and N-acetyl-L-cysteine (NAC) to reduce zinc deficiency induced oxidative stress, and prevent the activation of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1), and the cross-talk between both activated cascades through beta-Transducin Repeat containing Protein (beta-TrCP)."

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"At the molecular level, NAC has been shown to inhibit the activation of C Jun N-terminal kinase, p38 MAP kinase, redox sensitive activating protein-1 (AP-1) and the NF-kappaB transcriptional factor, thereby resulting in the suppression of numerous genes regulating the expression of many cytokines, such as TNF-alpha and IL-1 XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR."

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"Thus, NAC can inhibit activation of the JNK and c-Jun signaling pathway by reducing excessive ROS production, thereby reversing the cytotoxic effects of Dex."

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"NAC can inhibit activity of several signal transduction components such as nuclear factor kappa B, activator protein 1, and c- jun N-terminal kinase (JNK) by redox modulation [42, 43]."

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"NAC in combination with vanadate appeared to increase the efficacy of c-fos and c-jun inhibition, while decreasing toxicity."

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"As shown in xref , both 15(S)-HETE and 15(S)-HPETE upregulated the mRNA levels of c-FOS and c-JUN, which was inhibited by NAC."

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"showed that the administration of N-acetylocysteine (NAC), a ROS scavenger, reduced colonic cancer cell apoptosis via inhibition of JNK, p38 MAPK and activation of c-jun."