Abstract：
: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.
journal_name
Neurochem Intjournal_title
Neurochemistry internationalauthors
Niu L,Dai GH,He GL,Yang M,Hu HM,Liu ZK,Qian NS,Chen YLdoi
10.1016/j.neuint.2017.05.014subject
Has Abstractpub_date
2017-09-01 00:00:00pages
372-380eissn
0197-0186issn
1872-9754pii
S0197-0186(17)30140-7journal_volume
108pub_type
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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journal_title：Neurochemistry international
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