scholarly journals Effects of recombinant human erythropoietin on neuropathic pain and cerebral expressions of cytokines and nuclear factor-kappa B

2009 ◽  
Vol 56 (8) ◽  
pp. 597-603 ◽  
Author(s):  
Hong-bin Jia ◽  
Yi Jin ◽  
Qing Ji ◽  
Yi-feng Hu ◽  
Zhi-qiang Zhou ◽  
...  
2019 ◽  
Author(s):  
Zhi Ye ◽  
Qulian Guo ◽  
Xilei Li ◽  
E Wang ◽  
Wangyuan Zou ◽  
...  

Abstract Background: Nuclear factor kappa B is well-known for its pro-neuroinflammation function. However, it remains unknown how it increases the expression of inflammatory factors, which in turn promotes neuropathic pain. Here we investigated its role in the development of neuropathic pain in rats using a sciatic chronic constriction injury model and examined its effect in up-regulating CX3CR1 expression in BV-2 microglial cells induced by tumor necrosis factor-alpha. Methods : The sciatic nerve chronic constriction injury (CCI) model was used to induce neuropathic pain in rats. Mechanical stimuli and radiant heat were used to evaluate mechanical allodynia and thermal hyperalgesia. The pain related behavioral effect of Nuclear factor kappa B was accessed after intrathecal administration of pyrrolidine dithiocarbamate, a nuclear factor kappa B inhibitor. BV-2 microglia activation was induced by tumor necrosis factor-alpha incubation, and the levels of inflammatory factors and CX3CR1 were assessed. Results: Intrathecal infusion of pyrrolidine dithiocarbamate, a nuclear factor kappa B inhibitor, at 100 or 1000 pmol/d prevented the development of mechanical and thermal hyperalgesia and inhibited spinal microglial activation and tumor necrosis factor-alpha expression. In addition, phospho-p65 expression revealed that transient nuclear factor kappa B activation in BV-2 microglial cells was triggered by tumor necrosis factor-alpha.and increased CX3CR1 mRNA and protein expression. Pyrrolidine dithiocarbamate inhibited the tumor necrosis factor-alpha-inducedexpression of CX3CR1. Conclusion: These results suggested that the activation of nuclear factor kappa B pathway might enhance spinal microglial activation and tumor necrosis factor-alpha expression in neuropathic pain and the phosphorylation of p65 might be responsible for tumor necrosis factor-alpha-induced CX3CR1 expression in BV-2 microglial cells.


2001 ◽  
Vol 28 (6) ◽  
pp. 626-633 ◽  
Author(s):  
James R. Berenson ◽  
Hongjin M. Ma ◽  
Robert Vescio

2020 ◽  
Vol 19 (2) ◽  
pp. 164-171
Author(s):  
Feng Xue ◽  
Tingting Chen

Glioblastoma multiforme is the most common malignancy of central nervous system. Herein we have evaluated the effect of L-tetrahydropalmatine, an isoquinoline alkaloid, on the tumor growth both in vivo and in vitro using C6 glioblastoma multiforme cells and BALB/c mice injected subcutaneously with C6/luc2 cells. The results of these studies show that L-tetrahydropalmatine exhibited cytotoxic effect on C6 glioblastoma multiforme cells, suppressed nuclear factor-kappa B activity, suppressed the levels of tumor-linked proteins such as matrix metalloproteinase-2/9, Cyclin-D1, vascular endothelial growth factor, and X-linked inhibitor of apoptosis protein via ERK/nuclear factor-kappa B cascade. Further, L-tetrahydropalmatine inhibited the cell migration and invasion properties of C6 cells, and also suppressed the tumor weight and volume in mice. Immunohistochemical staining of tumor tissues suggested that L-tetrahydropalmatine inhibited the extracellular-signal-regulated kinase/nuclear factor-kappa B cascade and suppressed the levels of Cyclin-D1; matrix metalloproteinase-2/9; X-linked inhibitor of apoptosis protein; and vascular endothelial growth factor, and also the progression and growth of glioblastoma multiforme in mice. In summary, L-tetrahydropalmatine inhibits the ERK/nuclear factor-kappa B cascade, decreases the tumor volume, and inhibits the proteins responsible for tumor growth both in vivo and in vitro.


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