PubMed · 11953523
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Chris Pasero, Margo McCaffery. 2002. Monitoring sedation.. https://doi.org/10.1097/00000446-200202000-00026
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Morphine is frequently used for cancer patient's terminal medical care to relieve cancer pain. In the present study, we examined the inhibitory effect of morphine on experimental lung metastasis and invasion of colon 26-L5 cells. Morphine was found to significantly reduce the number of tumor colonies and the weight of the tumor-containing lung. Morphine inhibited the adhesion and migration of colon 26-L5 cells to extracellular matrix components and invasion into reconstituted basement membrane Matrigel, without affecting the cell proliferation in vitro. Notably, naloxone, an antagonist of morphine, abrogated morphine-induced inhibition of tumor cell adhesion, but did not affect the inhibitory effect on the production of matrix metalloproteinases (MMPs) from tumor cells. These results suggest that morphine inhibited the adhesive and invasive properties of tumor cells by different inhibitory mechanisms that involved the mediation of an opioid receptor.
Several novel racemic aminotetralin derivatives have been prepared using a stereoselective aziridine ring opening reactions and were evaluated for their micro-opioid receptor binding affinity. Selectivity index towards other opioid receptors and antinociceptive activity in mice have been evaluated for the most potent derivatives.
Modulation of opioid activity was accomplished for analogues of Leu-enkephalin through incorporation of a 4-imidazolidinone moiety. The peptide backbone was constrained via a methylene bridge between two neighboring amides within its regular peptide sequence, which was expected to disrupt the secondary structure of the original molecule. Five positional analogues of Leu-enkephalin based on the same sequence and different location of the imidazolidinone-constrict were designed, synthesized, and examined for their affinity to micro-, delta- and kappa-opioid receptors.