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Annals of Clinical & Laboratory Science 39:84-91 (2009)
© 2009 Association of Clinical Scientists

Recombinant Human Erythropoietin Attenuates Spinal Neuroimmune Activation of Neuropathic Pain in Rats

Hongbin Jia1, Xiaomei Feng2, Weiyan Li3, Yufeng Hu3, Qiong Zeng3, Jian Liu3 and Jianguo Xu3
1 Department of Anesthesiology, Jinling Hospital, Nanjing Clinical Medical College of the Second Military Medical University, Nanjing; 2 Department of Anesthesiology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai; 3 Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China

Address correspondence to Professor Jianguo Xu, Department of Anesthesiology, Jinling Hospital, 305 East Zhongshan Road, Nanjing 210002, P. R. China; tel 86 25 8480 6839; fax 86 25 5241 9949; e-mail jhb2121{at}163.com.

Neuropathic pain is a complex syndrome resulting from damage to the peripheral nervous system. Central neuroimmune activation contributes to the generation and maintenance of chronic pain after nerve injury. The current study determined the effects of recombinant human erythropoietin (rhEPO) on behavioral hyperalgesia and neuroimmune activation in a rat model of neuropathic pain induced by L5 spinal nerve transection. Animals were randomly assigned into 3 groups: sham-operation with saline; L5 spinal nerve transection with rhEPO (5000 units/kg); or L5 transection with saline. The rhEPO or saline was given ip on the day before surgery and continued daily to day 7 post-transection. The paw pressure threshold and paw withdrawal latencies were measured before surgery and on days 1, 3, and 7 post-operation. Glial activation markers such as macrophage antigen complex-1 (Mac-1, OX-42) and glial fibrillary acidic protein (GFAP), production of tumor necrosis factor (TNF)-{alpha}, interleukin (IL)-1β, and IL-10, as well as nuclear factor-kappa B (NF-{kappa}B) activation were determined in the lumbar spinal cord. Administration of rhEPO resulted in attenuation of mechanical and thermal hyperalgesia. Furthermore, rhEPO markedly inhibited neuroimmune activation characterized by glial activation, production of proinflammatory cytokines like TNF-{alpha}, IL-1β, and NF-{kappa}B activation, but rhEPO enhanced the level of IL-10. These results support the significance of neuroinflammation and neuroimmune activation in the initiation and persistence of behavioral pain responses. The data indicate that rhEPO attenuates behavioral hyperalgesia and neuroimmune activation in neuropathic pain induced by L5 nerve transection.

Keywords: rhEPO, neuropathic pain, astrocytes, microglia, inflammatory cytokines, NF-{kappa}B, TNF-{alpha}






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