Decreased spinal endomorphin-2 contributes to mechanical allodynia in streptozotocin-induced diabetic rats
| Autor: | Le Niu, Zhong-Kai Liu, Yong-Liang Chen, Nian-Song Qian, Hui-Min Hu, Guang-Hai Dai, Ming Yang, Gao-Le He |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty medicine.drug_class Receptors Opioid mu chemical and pharmacologic phenomena Streptozocin Diabetes Mellitus Experimental Rats Sprague-Dawley 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Diabetic Neuropathies Opioid receptor Internal medicine medicine Animals Opioid peptide Endogenous opioid Pain Measurement business.industry Chronic pain Cell Biology medicine.disease Streptozotocin Receptor antagonist Rats 030104 developmental biology Endocrinology Spinal Cord Hyperalgesia Anesthesia Neuropathic pain medicine.symptom business Oligopeptides 030217 neurology & neurosurgery medicine.drug |
| Zdroj: | Neurochemistry international. 108 |
| ISSN: | 1872-9754 |
| Popis: | Diabetic neuropathic pain (DNP) plays a major role in decreased life quality of diabetes patients, however, the neural mechanisms underlying DNP remain unclear. Endomorphins are the endogenous ligands for mu-opioid receptor. There is increasing evidence implicating the involvement of spinal endomorphin-2 (EM2) in neuropathic pain. In this study, using a streptozotocin induced diabetic rat model that displayed obvious mechanical allodynia, it was found that the expression of spinal EM2 was significantly decreased in DNP rats. While intrathecal administration of exogenous EM2 attenuated mechanical allodynia in DNP rats, the mu-opioid receptor antagonist β-funaltrexamine facilitated these events. It was found that the reduction in spinal EM2 was mediated by increased activity of dipeptidylpeptidase IV, possibly as a consequence of diabetes-induced oxidative stress. Taken together, our results provide the first evidence that the reduction in the level of an endogenous opioid in primary afferents was significantly associated with DNP. This indicates that the chronic pain associated with DNP might be due to the loss of an inhibitory effect on pain signal transmission. |
| Databáze: | OpenAIRE |
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