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Oxidative Medicine and Cellular Longevity
Volume 2012 (2012), Article ID 636419, 6 pages
Research Article

Oxidative Damage, Inflammation, and Toll-Like Receptor 4 Pathway Are Increased in Preeclamptic Patients: A Case-Control Study

1Laboratório de Fisiopatologia Experimental and Instituto Nacional Translacional em Medicina (INCT-TM), Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Avenida Universitária, 1105, 88806-000 Criciúma, SC, Brazil
2Laboratory of Exercise Biochemistry and Physiology, Graduate Program in Health Sciences, University of Southern Santa Catarina-UNESC, Criciúma, SC, Brazil

Received 10 February 2012; Revised 24 April 2012; Accepted 7 May 2012

Academic Editor: Neelam Khaper

Copyright © 2012 Fabiana C. B. Bernardi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Problem. There was no direct correlation between plasma and placental oxidative damage parameters and inflammation and evidence of TLR4 pathway activation in the placenta in preeclamptic (PE) patients. Method of Study. 33 PE patients and 33 normotensive pregnant women were included. The maternal section of the placenta and blood were collected to the determination of oxidative damage markers (thiobarbituric acid reactive species and protein carbonyls), inflammatory response (interleukin-6 and myeloperoxidase activity), and activation of the TLR-4-NF-kB pathway. Results. An increase of IL-6 levels in both plasma and placenta was observed, but myeloperoxidase activity was not significantly different comparing the groups. Oxidative damage parameters were increased in plasma and placenta in PE patients. A significant increase of the protein levels of TLR-4 and NF-kB was observed in the placenta. Conclusion. The TLR4-NF-kB pathway is upregulated in PE, probably generating local and systemic inflammatory response that is followed by local and systemic oxidative damage.