A Synthetic Cell-Penetrating Peptide Antagonizing TrkA Function Suppresses Neuropathic Pain in Mice

Journal of Pharmacological Sciences

Kenji Shigemi¹  Ming-Hui Cao²  Mineo Abe³  Wei-Ying Ma¹  Koyo Ueda¹  Yoshihiro Kuroda⁴  Eri Murata¹  Munetaka Hirose¹ 

[1] Department of Anesthesiology and Reanimatology, University of Fukui, Faculty of Medical Sciences, Japan;Department of Anesthesia, the Second Affiliated Hospital, Sun Yat-Sen University, China;Graduate School of Pharmaceutical Sciences, Kyoto University, Japan;Department of Pharmaceutical Health Care, Faculty of Pharmaceutical Sciences, Himeji Dokkyo University, Japan

关键词: cell-penetrating peptide;    neuropathic pain;    Tat;    TrkA;   

DOI  :  10.1254/jphs.10119FP

学科分类：药学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(24)Cited-By(5)Nerve growth factor (NGF) and its high-affinity receptor, TrkA, are one of the targets in the production of new drugs for the treatment of neuropathic pain. NGF contributes to both the initiation and maintenance of sensory abnormalities after peripheral nerve injury. This study examined the effects of IPTRK3, a new synthetic cell-penetrating peptide that antagonizes TrkA function, on neuropathic pain in mice. Partial sciatic nerve ligation (PSNL) was used to generate neuropathic pain, and we injected IPTRK3 (2 or 10 mg/kg) intraperitoneally on day 7 after PSNL. Effects of the peptide on hyperalgesia, allodynia, and expression of Fos in the spinal cord were examined. Single administration of the peptide on day 7 significantly suppressed both thermal hyperalgesia and mechanical allodynia. Gentle touch stimuli–evoked Fos expression in the lumbar spinal cord was also significantly reduced. Intraperitoneal injection of a cell-penetrating peptide antagonizing TrkA function appears effective for treatment of neuropathic pain in a mouse pain model.

【 授权许可】

Unknown