PubMed · 11719737
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
P Duvaldestin. 2001. Limited sampling approach.. https://doi.org/10.1016/s0009-9236(01)90137-7
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
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.
Administration of opioids that bind to the classical mu opioid receptor has been shown to lead to unintended alterations in immune function. Traditionally, altered immune function has been investigated with circulating immune cells. Effects of mu agonists on intestinal epithelial immune function have not been described. Since the oral route of administration is frequently employed with opiates, we determined if the mu receptor specific agonist endomorphin-1 altered interleukin-8 (IL-8) production by Caco-2 cells. Using RT-PCR and immunocytochemistry, Caco-2 cells were found to constitutively express (mu) mu opioid receptors. Activation of the mu receptor by endomorphin-1 (1 and 10 microM) resulted in significant increases in IL-8 when Caco-2 cells were stimulated with IL-1beta. Increased IL-8 secretion due to endomorphin-1 could be blocked by pre-incubating cells with the mu receptor antagonist, beta-funaltrexamine. These results indicate that the intestinal epithelial IL-8 response can be altered by a muopioid receptor mediated mechanism.
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.