The role of alpha-2 adrenoceptor subtype in the antiallodynic effect of intraplantar dexmedetomidine in a rat spinal nerve ligation model

2013 ◽  
Vol 557 ◽  
pp. 118-122 ◽  
Author(s):  
Hyung Gon Lee ◽  
Jeong Il Choi ◽  
Yeo Ok Kim ◽  
Myung Ha Yoon
Life Sciences ◽  
2013 ◽  
Vol 92 (4-5) ◽  
pp. 259-265 ◽  
Author(s):  
Ryohei Okazaki ◽  
Hiroyoshi Namba ◽  
Hiroyuki Yoshida ◽  
Hisashi Okai ◽  
Kazuki Taguchi ◽  
...  

2005 ◽  
Vol 18 (2) ◽  
pp. 118 ◽  
Author(s):  
Jun Gol Song ◽  
In Gu Jun ◽  
Mi Young Kwon ◽  
Jong Yeon Park

2012 ◽  
Vol 685 (1-3) ◽  
pp. 24-29 ◽  
Author(s):  
Tingjun Chen ◽  
Jianping Jiang ◽  
Hao Huang ◽  
Dongmei Wang ◽  
Yushan Liu ◽  
...  

2021 ◽  
Author(s):  
Yi-Hao Wang ◽  
Xiao Gao ◽  
Yu-Ru Tang ◽  
Nan-Nan Zhang ◽  
Zhao-Jun Liang ◽  
...  

Abstract Accumulated evidences have demonstrated causative links between neuropathic pain (NP) and immune-mediated inflammatory disorders. However, the role of inflammasome-induced pyroptosis in NP remains elusive. Melatonin possesses a well-documented analgesic action in various pain models. A rat model of spinal nerve ligation was established to explore the potential mechanism of melatonin in pyroptosis. The current study aimed to test our hypothesis that melatonin regulated pyroptosis to alleviate NP by inhibiting NF-κB/NLRP3-dependent signaling. Behavioral experiments revealed that SNL provoked severe allodynia which were suppressed by the administration of melatonin, caspase-1 inhibitor (VX-765) or NF-κB inhibitor (BAY 11-7085). SNL significantly up-regulated the inflammatory cytokines associated with the excessive activation of NLRP3 components and NF-κB signaling, as well as the marked pyroptosis activation which were partially inhibited by melatonin, VX-765 or BAY 11-7085. Collectively, Melatonin has potent analgesic and anti-inflammatory effects in SNL models through preventing pyroptosis via the NF-κB/NLRP3 inflammasome signaling pathway.


2003 ◽  
Vol 99 (5) ◽  
pp. 1175-1179 ◽  
Author(s):  
Xiaoying Zhu ◽  
James C. Eisenach

Background The mechanisms underlying neuropathic pain are incompletely understood and its treatment is often unsatisfactory. Spinal cyclooxygenase-2 (COX-2) expression is upregulated after peripheral inflammation, associated with spinal prostaglandin production leading to central sensitization, but the role of COX isoenzymes in sensitization after nerve injury is less well characterized. The current study was undertaken to determine whether COX-1 was altered in this model. Methods Male rats underwent partial sciatic nerve transsection (PSNT) or L5-L6 spinal nerve ligation (SNL). Four weeks after PSNT and 4 h, 4 days, or 2 weeks after SNL, COX-1 immunohistochemistry was performed on the L2-S2 spinal cord. Results COX-1 immunoreactivity (COX-1-IR) was unaffected 4 h after SNL. In contrast, 4 days after SNL, the number of COX-1-IR cells increased in the ipsilateral spinal cord. COX-1-IR increased in cells with glial morphology in the superficial laminae, but decreased in the rest of the ipsilateral spinal cord 4 weeks after PSNT and 2 weeks after SNL. These changes in immunostaining were greatest at the L5 level. Conclusion These data suggest that COX-1 expression in the spinal cord is not static, but changes in a time- and laminar-dependent manner after nerve injury. These anatomic data are consistent with observations by others that spinally administered specific COX-1 inhibitors may be useful to prevent and treat neuropathic pain.


2015 ◽  
Vol 11 ◽  
pp. s12990-015-0042 ◽  
Author(s):  
Jorge Baruch Pineda-Farias ◽  
Paulino Barragan-Iglesias ◽  
Emanuel Loeza-Alcocer ◽  
Jorge E Torres-Lopez ◽  
Héctor Isaac Rocha-Gonzalez ◽  
...  

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