Effect of thalidomide on signal transduction pathways and secondary damage in experimental spinal cord trauma

Shock
Tiziana GenoveseSalvatore Cuzzocrea

Abstract

TNF-alpha seems to play a central role in the inflammatory process of spinal cord injury. We tested the neuroprotective effects of thalidomide, an immunomodulatory agent that inhibits TNF-alpha production, which have not been investigated so far. The aim of our study was to evaluate the therapeutic efficacy of thalidomide in an experimental model of spinal cord trauma, which was induced by the application of vascular clips (force of 24 g) to the dura via a 4-level T5 to T8 laminectomy. Spinal cord injury in mice resulted in severe trauma characterized by edema, neutrophil infiltration, and cytokine production that is followed by recruitment of other inflammatory cells, production of a range of inflammation mediators, tissue damage, apoptosis, and disease. Thalidomide treatment significantly reduced the degree of: 1) spinal cord inflammation and tissue injury (histological score); 2) neutrophil infiltration (myeloperoxidase evaluation); 3) iNOS, nitrotyrosine, lipid peroxidation, and cytokine expression (TNF-alpha and IL-1beta); 4) apoptosis (terminal deoxynucleotidyltransferase-mediated UTP end labeling staining, and Bax and Bcl-2 expression); and 5) nuclear factor-kappaB activation. In a separate set of experiments, we have al...Continue Reading

References

Jun 1, 1979·Analytical Biochemistry·H OhkawaK Yagi
Apr 16, 1992·The New England Journal of Medicine·G B VogelsangJ R Wingard
Mar 1, 1991·The Journal of Experimental Medicine·E P SampaioG Kaplan
Apr 20, 1995·Nature·T ChittendenB C Guild
Aug 1, 1994·Brain : a Journal of Neurology·P K ThomasN H Wadia
Dec 1, 1993·Archives of Dermatology·A L HolmA A Gaspari
Jul 1, 1996·Chemical Research in Toxicology·J S Beckman
Jan 31, 1997·The Journal of Biological Chemistry·M MuzioV M Dixit
Jul 1, 1997·Journal of Neurochemistry·S HisaharaM Miura
Dec 6, 2000·Progress in Brain Research·D M McTigueB T Stokes
Jun 8, 2001·Journal of Neurotrauma·J XuC Y Hsu
Oct 16, 2001·European Journal of Clinical Pharmacology·T ErikssonP Höglund
Oct 18, 2001·BioDrugs : Clinical Immunotherapeutics, Biopharmaceuticals and Gene Therapy·C MeierhoferC J Wiedermann
Dec 18, 2002·Annals of the New York Academy of Sciences·Soo Hyun JinWon Ho Kim
Dec 25, 2002·Trends in Pharmacological Sciences·Phillip G Popovich, T Bucky Jones
Dec 19, 2003·Expert Opinion on Drug Safety·Emmanuel Laffitte, Jean Revuz
Jan 17, 2004·Lancet·William McBride
Oct 14, 2004·Annals of the Rheumatic Diseases·I M Verma
Jan 26, 2005·Journal of Neuroscience Research·O Nesic-TaylorJ R Perez-Polo
Feb 23, 2005·Current Pharmaceutical Design·Kozo YasuiKazunaga Agematsu
Aug 9, 2005·Journal of Neurotrauma·J Frederick HarringtonAdam Chodobski
Nov 24, 2005·The Journal of Pharmacology and Experimental Therapeutics·Tiziana GenoveseSalvatore Cuzzocrea
Aug 8, 2006·Biochemical and Biophysical Research Communications·Young Hwan AhnSoo Kyung Kang

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Citations

Jun 8, 2010·Journal of Molecular Histology·Chenyu ChuWeiquan Huang
Mar 5, 2011·Neurotherapeutics : the Journal of the American Society for Experimental NeuroTherapeutics·Swapan K RayNaren L Banik
Jan 21, 2014·Experimental Neurology·Stella Elkabes, Arnaud B Nicot
Dec 28, 2010·Trends in Pharmacological Sciences·Emanuela Esposito, Salvatore Cuzzocrea
Jul 6, 2016·Shock·Maximilian WenigerIrshad H Chaudry
Oct 16, 2015·Reviews in the Neurosciences·Mrinmay ChakrabartiSwapan K Ray
Aug 19, 2008·Shock·Christoph Thiemermann

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