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Discover Supplement-Drug Interactions

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Last Updated: 2 years ago

Possible Interaction: Acetylcysteine and Bardoxolone Methyl

Research Papers that Mention the Interaction

Pretreatment of cells with N-acetylcycsteine , a general purpose antioxidant or overexpression of glutathione peroxidase (GPx) or superoxide dismutase-1 (SOD-1) blocked the telomerase inhibitory activity of CDDO-Me.
Molecules  •  2013  |  View Paper
CDDO-Me inhibited the expression of prosurvival phospho-AKT (p-AKT), phospho-mammalian target of rapamycin (p-mTOR) and nuclear factor-kappa B (NF-κB) (…-2), B-cell lymphoma-extra large (BCL-xL), cellular inhibitor of apoptosis protein 1(c-IAP1) and survivin, but pre-treatment with NAC blocked ….
NAC also blocked the inhibition of cell proliferation by CDDO-Me.
Anticancer research  •  2013  |  View Paper
CDDO-Me down-regulated p-Akt, p-mTOR and NF-kappaB (p65) but increased the activation of Erk1/2 and NAC blocked the modulation of these cell signaling proteins by CDDO-Me.
Likewise, NAC prevented the induction of apoptosis (annexin V-FITC binding and cleavage of PARP-1 and procaspases-3,-8 and -9) and reversed the loss of mitochondrial membrane potential and release of cytochrome c from mitochondria by CDDO-Me.
Pretreatment with N-acetylcysteine (NAC) or overexpression of glutathione peroxidase (GPx) or superoxide dismutase-1 (SOD-1) blocked the antiproliferative effects of CDDO-Me.
Journal of experimental therapeutics & oncology  •  2012  |  View Paper
CDDO-Me caused the generation of reactive oxygen species, which was inhibited by NAC and mitochondrial chain 1 complex inhibitors DPI and rotenone.
CDDO-Me induced apoptosis as demonstrated by the cleavage of PARP-1, activation of procaspases -3, -8, and -9 and mitochondrial depolarization and NAC blocked the activation of these apoptosis related processes.
Results demonstrated that CDDO-Me potently inhibited the growth of colorectal cancer cells and pretreatment of cancer cells with small-molecule antioxidant N-acetylcysteine ( NAC ) completely blocked the growth inhibitory activity of CDDO-Me.
Journal of experimental therapeutics & oncology  •  2011  |  View Paper
NAC also prevented the inhibition of constitutively active Akt, NF-kappaB and mTOR by CDDO-Me.
Pretreatment with NAC blocked annexin V-binding, cleavage of PARP-1 and procaspases-3, -8, -9, loss of mitochondrial membrane potential and release of cytochrome c by CDDO-Me.
Biochemical pharmacology  •  2010  |  View Paper
The anti-oxidant N-acetyl cysteine NAC ) could overcome this AR-suppressive effect of CDDO-Me.
Antioxidants  •  2020  |  View Paper