Study on the molecular mechanism of antinociception induced by ghrelin in acute pain in mice |
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| Institution: | 1. Department of Physiology, Medical College of Nanchang University, Bayi Road 461, Nanchang, Jiangxi, 330006, China;2. Medical Experimental Teaching Department, Nanchang University, Nanchang 330031, China;1. Department of Pathophysiology, Faculty of Medicine, University of Szeged, Hungary;2. Institute of Laboratory Medicine, Faculty of Medicine, University of Szeged, Hungary;1. Department of Anesthesiology, Heidelberg University Hospital, Heidelberg, Germany;2. Clinic for Anesthesiology, Intensive Care and Emergency Medicine I, Westpfalz Hospital, Kaiserslautern, Germany;1. Univ. Bordeaux, F-33076 Bordeaux, France;2. INSERM U1035, F-33076 Bordeaux, France;3. Bordeaux INP, BPRVS, EA4135, F-33000 Bordeaux, France;4. CNRS UMS 3427, F-33076 Bordeaux, France;1. Departments of Neurosurgery, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung;2. Department of Anesthesiology, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan;3. Department of Neurosurgery, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan;4. Department of Microbiology, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan;5. Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan;1. College of Medicine, Graduate Institute of Basic Medical Science, China Medical University, Taichung 404, Taiwan;2. College of Chinese Medicine, School of Post-Baccalaureate Chinese Medicine, China Medical University, Taichung 404, Taiwan;3. College of Agriculture and Natural Resources, Graduate Institute of Biotechnology, National Chung Hsing University, Taichung 402, Taiwan;4. College of Biotechnology, Institute of Nanoengineering and Microsystems, National Tsing Hua University, Hsinchu 300, Taiwan;5. College of Chinese Medicine, Graduate Institute of Acupuncture Science, China Medical University, Taichung 404, Taiwan;6. Research Center for Chinese Medicine & Acupuncture, China Medical University, Taichung 404, Taiwan;1. Department of Pharmaceutical Biosciences, Uppsala University, Uppsala, Sweden;2. Moscow State University, Moscow, Russia;3. Tauber Bioinformatics Research Center, University of Haifa, Haifa, Israel;4. Department of Molecular Oncogenetics, Institute of Molecular Biology and Genetics, Kiev, Ukraine;5. Department of Human Genetics, Institute of Molecular Biology and Genetics, Kiev, Ukraine;6. Higher School of Economics, Moscow, Russia;7. Department of Clinical Sciences, Division of Neurosurgery, University Hospital of Southern Sweden, Lund University, Lund, Sweden;8. Department of Pharmacology, University of Arizona Health Sciences Center, Tucson, AZ, United States |
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| Abstract: | Ghrelin has been identified as the endogenous ligand for the GHS-R1α (growth hormone secretagogue receptor 1 alpha). Our previous experiments have indicated that ghrelin (i.c.v.) induces antinociceptive effects in acute pain in mice, and the effects were mediated through the central opioid receptors and GHS-R1α. However, which opioid receptor (OR) mediates the antinociceptive effects and the molecular mechanisms are also needed to be further explored. In the present study, the antinociceptive effects of ghrelin (i.c.v.) could be fully antagonized by δ-opioid receptor antagonist NTI. Furthermore, the mRNA and protein levels of δ-opioid peptide PENK and δ-opioid receptor OPRD were increased after i.c.v injection of ghrelin. Thus, it showed that the antinociception of ghrelin was correlated with the GHS-R1α and δ-opioid receptors. To explore which receptor was firstly activated by ghrelin, GHS-R1α antagonist D-Lys3]-GHRP-6 was co-injection (i.c.v.) with deltorphin II (selective δ-opioid receptor agonist). Finally, the antinociception induced by deltorphin II wasn’t blocked by the co-injection (i.c.v.) of D-Lys3]-GHRP-6, indicating that the GHS-R1α isn’t on the backward position of δ-opioid receptor. The results suggested that i.c.v. injection of ghrelin initially activated the GHS-R1α, which in turn increased the release of endogenous PENK to activation of OPRD to produce antinociception. |
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