Display options
Cite
Lv R, Xu X, Luo Z, et al. Pyrrolidine dithiocarbamate (PDTC) inhibits the overexpression of MCP-1 and attenuates microglial activation in the hippocampus of a pilocarpine-induced status epilepticus rat model. Exp Ther Med. 2013;7(1):39-45doi: 10.3892/etm.2013.1397.
Lv, R., Xu, X., Luo, Z., Shen, N., Wang, F., & Zhao, Y. (2014). Pyrrolidine dithiocarbamate (PDTC) inhibits the overexpression of MCP-1 and attenuates microglial activation in the hippocampus of a pilocarpine-induced status epilepticus rat model. Experimental and therapeutic medicine, 7(1), 39-45. https://doi.org/10.3892/etm.2013.1397
Lv, Rilang, et al. "Pyrrolidine dithiocarbamate (PDTC) inhibits the overexpression of MCP-1 and attenuates microglial activation in the hippocampus of a pilocarpine-induced status epilepticus rat model." Experimental and therapeutic medicine vol. 7,1 (2014): 39-45. doi: https://doi.org/10.3892/etm.2013.1397
Lv R, Xu X, Luo Z, Shen N, Wang F, Zhao Y. Pyrrolidine dithiocarbamate (PDTC) inhibits the overexpression of MCP-1 and attenuates microglial activation in the hippocampus of a pilocarpine-induced status epilepticus rat model. Exp Ther Med. 2014 Jan;7(1):39-45. doi: 10.3892/etm.2013.1397. Epub 2013 Nov 08. PMID: 24348761; PMCID: PMC3861516.
Copy Download .nbib Format: NLM
Share it on

Exp Ther Med. 2014 Jan;7(1):39-45. doi: 10.3892/etm.2013.1397. Epub 2013 Nov 08.

Pyrrolidine dithiocarbamate (PDTC) inhibits the overexpression of MCP-1 and attenuates microglial activation in the hippocampus of a pilocarpine-induced status epilepticus rat model.

Experimental and therapeutic medicine

Rilang Lv, Xiaoyun Xu, Zheng Luo, Nan Shen, Feng Wang, Yongbo Zhao

Affiliations

  1. Department of Neurology, Shanghai East Hospital Affiliated to Tongji University School of Medicine, Shanghai 200210, P.R. China.
  2. Department of Neurology, Shanghai East Hospital Affiliated to Tongji University School of Medicine, Shanghai 200210, P.R. China ; Department of Neurology, Shanghai Pudong New Area Zhoupu Hospital, Shanghai 201318, P.R. China.
  3. Department of Neurology, Shanghai Jiaotong University Affiliated First People's Hospital, Shanghai 200080, P.R. China.

PMID: 24348761 PMCID: PMC3861516 DOI: 10.3892/etm.2013.1397

Abstract

The aim of this study was to investigate the effects of pyrrolidine dithiocarbamate (PDTC) on MCP-1 expression and microglial activation in the hippocampus of a rat model of pilocarpine (PILO)-induced status epilepticus (SE). Moreover, seizure susceptibility, frequency and severity as well as brain damage were analyzed and changes in behavior were recorded. Chemokine MCP-1 expression and microglial activation were detected by immunohistochemistry (IHC). Fluoro-Jade C (FJC) and NeuN staining were used for the evaluation of tissue damage. Our results showed that although SE resulted in the upregulation of MCP-1 and microglial activation in the rat hippocampus 24 h after seizure onset, pretreatment with PDTC significantly inhibited the MCP-1 overexpression and attenuated the microglial activation. These effects were accompanied by neurodegenerative amelioration. To the best of our knowledge, these findings indicated for the first time that the activation of the nuclear factor-κB (NF-κB) pathway may contribute to MCP-1 upregulation and microglial activation in the context of epilepsy. PDTC was also shown to exert anticonvulsant activity and to have a neuroprotective effect on the hippocampal CA1 and CA3 regions, potentially through attenuating microglial activation.

Keywords: MCP-1 (CCL2); epilepsy; hippocampus; nuclear factor-κB; pilocarpine-induced status epilepticus rat model; pyrrolidine dithiocarbamate

References

  1. Acta Pharmacol Sin. 2011 Feb;32(2):188-93 - PubMed
  2. Science. 2005 May 6;308(5723):778-81 - PubMed
  3. Exp Neurol. 2002 Dec;178(2):294-300 - PubMed
  4. Curr Top Med Chem. 2012;12(9):1008-32 - PubMed
  5. J Neurochem. 2007 Nov;103(4):1381-95 - PubMed
  6. Electroencephalogr Clin Neurophysiol. 1972 Mar;32(3):281-94 - PubMed
  7. FASEB J. 2011 Feb;25(2):737-53 - PubMed
  8. Epilepsia. 2011 May;52 Suppl 3:1-4 - PubMed
  9. J Neuroinflammation. 2011 May 02;8:41 - PubMed
  10. J Neuroinflammation. 2009 Dec 24;6:40 - PubMed
  11. J Neurosci Res. 2010 Jul;88(9):1898-907 - PubMed
  12. J Neurochem. 2007 Feb;100(4):1072-88 - PubMed
  13. Brain Res. 2008 Nov 19;1241:157-67 - PubMed
  14. Mol Med. 2007 Jan-Feb;13(1-2):1-13 - PubMed
  15. Epilepsia. 2008;49 Suppl 2:33-41 - PubMed
  16. Free Radic Biol Med. 2006 May 15;40(10):1776-84 - PubMed
  17. Epilepsy Res. 2009 Dec;87(2-3):177-83 - PubMed
  18. Brain Res. 2007 Nov 28;1182:138-43 - PubMed
  19. J Neurol Sci. 2011 Sep 15;308(1-2):25-7 - PubMed
  20. Mol Cells. 2002 Jun 30;13(3):429-35 - PubMed
  21. Prog Neurobiol. 1999 Apr;57(6):563-81 - PubMed
  22. J Neuroimmunol. 2011 May;234(1-2):93-102 - PubMed
  23. Neuropharmacology. 2013 Jun;69:16-24 - PubMed
  24. Neuroscience. 2011 Jul 28;187:93-102 - PubMed
  25. J Neurosci Res. 2007 Nov 1;85(14):3150-9 - PubMed
  26. Curr Biol. 1998 Jan 1;8(1):19-25 - PubMed
  27. J Comp Neurol. 2005 Nov 14;492(2):178-92 - PubMed
  28. Am J Pathol. 2012 May;180(5):1950-62 - PubMed
  29. Am J Kidney Dis. 2000 Dec;36(6):1226-41 - PubMed
  30. Epilepsia. 2005;46 Suppl 5:113-7 - PubMed
  31. Pathophysiology. 2013 Feb;20(1):59-69 - PubMed
  32. Clin Neuropathol. 2008 Mar-Apr;27(2):55-63 - PubMed
  33. Clin Exp Pharmacol Physiol. 2004 May-Jun;31(5-6):320-6 - PubMed
  34. J Neuroimmunol. 2010 Jul 27;224(1-2):22-7 - PubMed
  35. Acta Neurobiol Exp (Wars). 2011;71(2):193-207 - PubMed
  36. Mediators Inflamm. 2011;2011:670613 - PubMed
  37. Clin Chim Acta. 2010 Nov 11;411(21-22):1570-9 - PubMed
  38. J Neurosci. 2007 Feb 14;27(7):1738-45 - PubMed
  39. Int Heart J. 2010;51(5):348-53 - PubMed
  40. J Neurosci. 1999 Jun 15;19(12):5054-65 - PubMed
  41. J Neuroinflammation. 2010 Oct 12;7:65 - PubMed
  42. Neurobiol Dis. 2012 May;46(2):425-30 - PubMed

Publication Types