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Discover Supplement-Drug Interactions
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Last Updated: 3 years ago
supplement:
Gamma-Aminobutyric Acid
drug:
Nicotine
Research Papers that Mention the Interaction
“In vitro exposure of cells to single doses or seven days of nicotine induced the protein expression of MMP-2, MMP-9 and EGR-1 and these responses were blocked by GABA.”
Differential modulation of nicotine-induced gemcitabine resistance by GABA receptor agonists in pancreatic cancer cell xenografts and in vitro“Both in vivo and in vitro the administration of nicotine stimulated an overflow of aspartate, glutamate and GABA.”
“Interestingly, GABA , being an antagonist to cAMP signaling, showed a promising intervention by reversing the stimulatory effect of nicotine on cancer growth and all signaling pathways.”
“However, other neurochemical systems also participate in the addictive effects of nicotine including glutamate, cannabinoids, GABA and opioids.”
“Accordingly, pharmacological agents that target brain acetylcholine, DA, glutamate, GABA , or endocannabonoid signaling systems have been proposed to interrupt nicotine action.”
“ Nicotine additionally reduced the protein levels of both GAD isozymes and GABA in tumor tissue.”
“Treatment with GABA abolished these responses to nicotine and blocked the development of xenografts in mice not exposed to nicotine.”
“Our data suggest that nicotine increases the SHH-mediated malignant potential of PCSCs and that GABA prevents these effects.”
“ Nicotine treatment also down-regulated expression of the GABA synthesizing enzyme GAD 65 and the level of endogenous GABA, while treatment of NSCLC cells with GABA inhibited cell proliferation.”
“All of the observed adverse effects of chronic nicotine were reversed by treatment of the cells with γ-aminobutyric acid , suggesting the potential usefulness of this agent for the improvement of PDAC intervention strategies in smokers.”
“Second, we discuss preclinical evidence that suggests nicotine affects GABA neuronal function indirectly by a primary action at neuronal nicotinic acetylcholine receptors.”
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