Intrathecal injection of anti-CX3CR1 neutralizing antibody delayed and attenuated pain facilitation in rat tibial bone cancer pain model

2010 ◽  
Vol 21 (7) ◽  
pp. 595-601 ◽  
Author(s):  
Qin Yin ◽  
Wei Cheng ◽  
Ming-Yue Cheng ◽  
Su-Zhen Fan ◽  
Wen Shen
2015 ◽  
Vol 172 (8) ◽  
pp. 2148-2164 ◽  
Author(s):  
Keiko Takasu ◽  
Koichi Ogawa ◽  
Atsushi Nakamura ◽  
Tomoe Kanbara ◽  
Hiroko Ono ◽  
...  

2004 ◽  
Vol 79 (2) ◽  
pp. 243-251 ◽  
Author(s):  
Hilde Vermeirsch ◽  
Rony M. Nuydens ◽  
Philip L. Salmon ◽  
Theo F. Meert

2011 ◽  
Vol 5 (1) ◽  
pp. 221
Author(s):  
V.P. Gutierrez ◽  
P. Brigatte ◽  
V.O. Zambelli ◽  
G. Picolo ◽  
J.S.D. Carvalho ◽  
...  

PPAR Research ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Jie Fu ◽  
Baoxia Zhao ◽  
Chaobo Ni ◽  
Huadong Ni ◽  
Longsheng Xu ◽  
...  

Bone cancer pain (BCP) is a serious clinical problem that affects the quality of life of cancer patients. However, the current treatment methods for this condition are still unsatisfactory. This study investigated whether intrathecal injection of rosiglitazone modulates the noxious behaviors associated with BCP, and the possible mechanisms related to this effect were explored. We found that rosiglitazone treatment relieved bone cancer-induced mechanical hyperalgesia in a dose-dependent manner, promoted the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) in spinal cord neurons, and inhibited the activation of the nuclear factor-kappa B (NF-κB)/nod-like receptor protein 3 (NLRP3) inflammatory axis induced by BCP. However, concurrent administration of the PPAR-γ antagonist GW9662 reversed these effects. The results show that rosiglitazone inhibits the NF-κB/NLRP3 inflammation axis by activating PPAR-γ in spinal neurons, thereby alleviating BCP. Therefore, the PPAR-γ/NF-κB/NLRP3 signaling pathway may be a potential target for the treatment of BCP in the future.


2014 ◽  
Vol 125 (3) ◽  
pp. 264-273 ◽  
Author(s):  
Hiroko Ono ◽  
Atsushi Nakamura ◽  
Tomoe Kanbara ◽  
Kazuhisa Minami ◽  
Shunji Shinohara ◽  
...  

2006 ◽  
pp. 287-289
Author(s):  
Darryl T. Hamamoto ◽  
Donald A. Simone

2013 ◽  
Vol 119 (5) ◽  
pp. 1178-1185 ◽  
Author(s):  
Dorothy Cimino Brown ◽  
Kimberly Agnello

Abstract Background: Substance P-saporin (SP-SAP), a chemical conjugate of substance P and a recombinant version of the ribosome-inactivating protein, saporin, when administered intrathecally, acts as a targeted neurotoxin producing selective destruction of superficial neurokinin-1 receptor–bearing cells in the spinal dorsal horn. The goal of this study was to provide proof-of-concept data that a single intrathecal injection of SP-SAP could safely provide effective pain relief in spontaneous bone cancer pain in companion (pet) dogs. Methods: In a single-blind, controlled study, 70 companion dogs with bone cancer pain were randomized to standard-of-care analgesic therapy alone (control, n = 35) or intrathecal SP-SAP (20–60 µg) in addition to standard-of-care analgesic therapy (n = 35). Activity, pain scores, and videography data were collected at baseline, 2 weeks postrandomization, and then monthly until death. Results: Although the efficacy results at the 2-week postrandomization point were equivocal, the outcomes evaluated beyond 2 weeks revealed a positive effect of SP-SAP on chronic pain management. Significantly, more dogs in the control group (74%) required unblinding and adjustment in analgesic protocol or euthanasia within 6 weeks of randomization than dogs that were treated with SP-SAP (24%; P < 0.001); and overall, dogs in the control group required unblinding significantly sooner than dogs that had been treated with SP-SAP (P < 0.01). Conclusion: Intrathecal administration of SP-SAP in dogs with bone cancer produces a time-dependent antinociceptive effect with no evidence of development of deafferentation pain syndrome which can be seen with neurolytic therapies.


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