| First Author | Yamacita-Borin FY | Year | 2015 |
| Journal | Neurosci Lett | Volume | 605 |
| Pages | 53-8 | PubMed ID | 26291484 |
| Mgi Jnum | J:228438 | Mgi Id | MGI:5707096 |
| Doi | 10.1016/j.neulet.2015.08.015 | Citation | Yamacita-Borin FY, et al. (2015) Superoxide anion-induced pain and inflammation depends on TNFalpha/TNFR1 signaling in mice. Neurosci Lett 605:53-8 |
| abstractText | Inhibition of tumor necrosis factor-alpha (TNFalpha) and superoxide anion production reduces inflammation and pain. The present study investigated whether superoxide anion-induced pain depends on TNFalpha signaling and the role of superoxide anion in TNFalpha-induced hyperalgesia to clarify the interrelation between these two mediators in the context of pain. Intraplantar injection of a superoxide anion donor (potassium superoxide) induced mechanical hyperalgesia (0.5-5h after injection), neutrophil recruitment (myeloperoxidase activity), and overt pain-like behaviors (paw flinching, paw licking, and abdominal writhings) in wild-type mice. Tumor necrosis factor receptor 1 deficiency (TNFR1-/-) and treatment of wild-type mice with etanercept (a soluble TNFR2 receptor that inhibits TNFalpha actions) inhibited superoxide anion-induced pain-like behaviors. TNFR1(-/-) mice were also protected from superoxide anion donor-induced oxidative stress, suggesting the role of this pathway in the maintenance of oxidative stress. Finally, we demonstrated that Apocynin (an NADPH oxidase inhibitor) or Tempol (a superoxide dismutase mimetic) treatment inhibited TNFalpha-induced paw mechanical hyperalgesia and neutrophil recruitment (myeloperoxidase activity). These results demonstrate that TNFalpha/TNFR1 signaling is important in superoxide anion-triggered pain and that TNFalpha/TNFR1 signaling amplifies the oxidative stress triggered by superoxide anion, which contributes to sustaining pain and inflammation. |
