Upregulation of Inflammatory Mediators in a Model of Chronic Pain after Spinal Cord Injury |
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Authors: | Rajat Sandhir Eugene Gregory Yong-Yue He Nancy E J Berman |
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Institution: | (1) Steve Palermo Nerve Regeneration Laboratory, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA;(2) Department of Anatomy and Cell Biology, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA;(3) Department of Neurosurgery, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA;(4) Hoglund Brain Imaging Center, University of Kansas Medical Center, 3901 Rainbow Boulevard, Kansas City, KS 66160, USA; |
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Abstract: | Chronic neuropathic pain is a disabling condition observed in large number of individuals following spinal cord injury (SCI).
Recent progress points to an important role of neuroinflammation in the pathogenesis of central neuropathic pain. The focus
of the present study is to investigate the role of proinflammatory molecules IL-1β, TNF-α, MCP-1, MMP-9 and TIMP-1 in chronic
neuropathic pain in a rodent model of SCI. Rats were subjected to spinal cord contusion using a controlled linear motor device
with an injury epicenter at T10. The SCI rats had severe impairment in locomotor function at 7 days post-injury as assessed
by the BBB score. The locomotor scores showed significant improvement starting at day 14 and thereafter showed no further
improvement. The Hargreaves’ test was used to assess thermal hyperalgesia for hindpaw, forepaw and tail. A significant reduction
in withdrawal latency was observed for forepaw and tail of SCI rats at days 21 and 28, indicating the appearance of thermal
hyperalgesia. Changes in expression of mRNAs for IL-1β, TNF-α, MCP-1, MMP-9 and TIMP-1 were assessed using real-time polymerase
chain reaction in spinal cord including the injury epicenter along with regions above and below the level of lesion at day
28 post-injury. A significant increase was observed in the expression of MCP-1, TNF-α, TIMP-1 and IL-1β in the injury epicenter,
whereas only TIMP-1 was upregulated in the area below the injury epicenter. The results of the study suggest that prolonged
upregulation of inflammatory mediators might be involved in chronic neuropathic pain in SCI, and that TIMP-1 may play a role
in maintenance of chronic below level pain. |
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