A minocycline derivative reduces nerve injury-induced allodynia, LPS-induced prostaglandin E2 microglial production and signaling via toll-like receptors 2 and 4.

@article{Bastos2013AMD,
  title={A minocycline derivative reduces nerve injury-induced allodynia, LPS-induced prostaglandin E2 microglial production and signaling via toll-like receptors 2 and 4.},
  author={Leandro Francisco Silva Bastos and Adriana Martins Godin and Yingning Zhang and Suwatchai Jarussophon and Bruno Christiano Silva Ferreira and Renes de Resende Machado and Steven F. Maier and Yasuo Konishi and Rossimiriam Pereira de Freitas and Bernd L. Fiebich and Linda R. Watkins and M{\'a}rcio de Matos Coelho and M{\'a}rcio Fl{\'a}vio Dutra Moraes},
  journal={Neuroscience letters},
  year={2013},
  volume={543},
  pages={157-62}
}
Many studies have shown that minocycline, an antibacterial tetracycline, suppresses experimental pain. While minocycline's positive effects on pain resolution suggest that clinical use of such drugs may prove beneficial, minocycline's antibiotic actions and divalent cation (Ca(2+); Mg(2+)) chelating effects detract from its potential utility. Thus, we tested the antiallodynic effect induced by a non-antibacterial, non-chelating minocycline derivative in a model of neuropathic pain and performed… CONTINUE READING

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