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Last Updated: 3 years ago

Possible Interaction: Nicotine and Tubocurarine

supplement:

Tubocurarine

Research Papers that Mention the Interaction

The effect of nicotine exposure on surfactant gene expression is apparently mediated by nicotinic acetylcholine receptors because it was blocked by D-tubocurarine.
The American journal of physiology  •  1998  |  View Paper
4 Dihydro‐β‐erythroidine (DHBE) and tubocurarine antagonized both ACh and nicotine excitations but not those induced by glutamate or dl‐homocysteic acid.
British journal of pharmacology  •  1976  |  View Paper
T-REx293 cells expressed the nicotinic acetylcholine receptor (nAchR) and tubocurarine , an nAChR antagonist, completely blocked the effects of nicotine.
The Journal of toxicological sciences  •  2018  |  View Paper
The increased cell proliferation and gene upregulation induced by nicotine were inhibited by addition of the nicotinic receptor antagonist d-tubocurarine.
Journal of Bone and Mineral Metabolism  •  2009  |  View Paper
Enhancement of MMP-1 expression by nicotine treatment was eliminated by simultaneous treatment with D-tubocurarine.
Acta biochimica et biophysica Sinica  •  2006  |  View Paper
Mecamylamine (10 μM), dihydro‐β‐erythroidine (10 μM) and d‐tubocurarine (30 μM), but not α‐bungarotoxin (α‐BTX, 0.1 μM), attenuated the NIC (100 μM)‐evoked release of [3H]‐NA.
British journal of pharmacology  •  2002  |  View Paper
In addition, we demonstrate direct cellular effects of nicotine on primary human bone cells and blockage of these effects with a nicotinic receptor antagonist, D-tubocurarine.
Bone  •  2001  |  View Paper
The facilitatory effect of nicotine was prevented by 30 µM (+)-tubocurarine.
Naunyn-Schmiedeberg's Archives of Pharmacology  •  2001  |  View Paper
The increase in tau immunoreactivity induced by nicotine , epibatidine, and tacrine, but not the up‐regulation of nAChRs, was prevented by the antagonists d‐tubocurarine and mecamylamine.
Journal of neurochemistry  •  2000  |  View Paper
The effect of nicotine on up-regulation of alpha7 AChRs was partially blocked by either d-tubocurarine or mecamylamine.
The effect of nicotine treatment on the number of alpha3 AChRs was only slightly blocked by the antagonists d-tubocurarine , mecamylamine, or dihydro-beta-erythroidine at concentrations that efficiently block alpha3 AChR function.
Molecular pharmacology  •  1997  |  View Paper
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