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pharmazentrum frankfurt, Institut für Klinische Pharmakologie, Klinikum der Johann Wolfgang Goethe-Universität Frankfurt, Germany
Abstract
Abstract I. Introduction II. Growth-Promoting and Protective Effects A. G{beta}{gamma}-Phosphatidylinositol 3-Kinase Pathway B. Calmodulin—Epidermal Growth Factor Receptor Pathway C. µ3-Opioid Receptor—Nitric Oxide Pathway III. Death-Promoting and Antiproliferative Effects A. Hormone-Mediated Effects B. Chemokine- and Cytokine-Mediated Effects C. Apoptosis Associated with Tolerance D. Is Cell Death Initiated by Receptor Desensitization E. Direct Effects of Internalized Agonist F. {beta}-Arrestin As Signal Transducer IV. Summary of Mechanisms of Action V. Clinical Implications A. Inhibition of Inflammation with Endogenous Opioids B. Morphine Plus Naloxone As Add-On for Cancer Treatment C. Subanalgesic Morphine to Accelerate Healing Processes
Opioids are powerful analgesics but also drugs of abuse. Because opioid addicts are susceptible to certain infections, opioids have been suspected to suppress the immune response. This was supported by the finding that various immune-competent cells express opioid receptors and undergo apoptosis when treated with opioid alkaloids. Recent evidence suggests that opioids may also effect neuronal survival and proliferation or migrating properties of tumor cells. A multitude of signaling pathways has been suggested to be involved in these extra-analgesic effects of opioids. Growth-promoting effects were found to be mediated through Akt and Erk signaling cascades. Death-promoting effects have been ascribed to inhibition of nuclear factor-
B, increase of Fas expression, p53 stabilization, cytokine and chemokine release, and activation of nitric oxide synthase, p38, and c-Jun-N-terminal kinase. Some of the observed effects were inhibited with opioid receptor antagonists or pertussis toxin; others were unaffected. It is still unclear whether these properties are mediated through typical opioid receptor activation and inhibitory G-protein-signaling. The present review tries to unravel controversial findings and provides a hypothesis that may help to integrate diverse results.
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