Role of Dehydrocorybulbine in Neuropathic Pain After Spinal Cord Injury Mediated by P2X4 Receptor
Zhongwei Wang1,2, Wei Mei2, Qingde Wang2, Rundong Guo2, Peilin Liu2, Yuqiang Wang1, Zijuan Zhang3, and Limin Wang1,*
1Department of Orthopaedics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China, 2Department of Spine Surgery, Zhengzhou Orthopaedic Hospital, Zhengzhou, China, 3Experimental Teaching Center, School of Basic Medical Science, Henan University of Chinese Medicine, Zhengzhou, China
*Correspondence: fccwangyq2@zzu.edu.cn
Received January 1, 2018; Revised August 13, 2018; Accepted August 27, 2018.; Published online January 2, 2019.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

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ABSTRACT
Chronic neuropathic pain is one of the primary causes of disability subsequent to spinal cord injury. Patients experiencing
neuropathic pain after spinal cord injury suffer from poor quality of life, so complementary therapy is seriously needed.
Dehydrocorybulbine is an alkaloid extracted from Corydalis yanhusuo. It effectively alleviates neuropathic pain. In the
present study, we explored the effect of dehydrocorybulbine on neuropathic pain after spinal cord injury and delineated its
possible mechanism. Experiments were performed in rats to evaluate the contribution of dehydrocorybulbine to P2X4
signaling in the modulation of pain-related behaviors and the levels of pronociceptive interleukins and proteins after spinal
cord injury. In a rat contusion injury model, we confirmed that chronic neuropathic pain is present on day 7 after spinal cord
injury and P2X4R expression is exacerbated after spinal cord  injury. We also found that administration of dehydrocorybulbine by tail vein injection relieved pain behaviors in rat contusion injury models without affecting motor functions. The elevation in the levels of pronociceptive interleukins (IL-1β, IL-18, MMP-9) after spinal cord injury was mitigated by dehydrocorybulbine. Dehydrocorybulbine significantly mitigated the upregulation of P2X4 receptor and reduced ATP-evoked intracellular Ca2+ concentration. Both P2XR and dopamine receptor2 agonists antagonized dehydrocorybulbine’s antinociceptive effects. In conclusion, we propose that dehydrocorybulbine produced antinociceptive effects in spinal cord injury models by inhibiting P2X4R.
Keywords: dehydrocorybulbine, P2X4, Pain, Spinal cord injury


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31 December 2018 Volume 41,
Number 12, pp. 993~1081

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