Protective Effect of Vitamin E in an Animal Model of LPS-Induced Inflammation
Article first published online: 14 DEC 2004
American Journal of Reproductive Immunology
Volume 52, Issue 6, pages 356–361, December 2004
How to Cite
Mayorga, M., Iborra, A., Estany, S. and Martínez, P. (2004), Protective Effect of Vitamin E in an Animal Model of LPS-Induced Inflammation. American Journal of Reproductive Immunology, 52: 356–361. doi: 10.1111/j.1600-0897.2004.00233.x
- Issue published online: 14 DEC 2004
- Article first published online: 14 DEC 2004
- Submitted March 19, 2002; revised July 20, 2004; accepted September 17, 2004.
- embryo viability;
- inflammatory response;
- oxidative stress
Problem: Many sterility outcomes may be associated to the presence of an inflammatory response that would lead to an inability of the endometrium to support implantation and maintain viable embryos. We have established an animal model of inflammation in which the systemic administration of lipopolysaccharyde (LPS) results in a low embryo implantation rate. The purpose of this work was to investigate the effect of the inflammatory agent LPS on embryo viability and to verify the ability of vitamin E to modulate the inflammatory effect of LPS on embryo viability.
Method of study: For pre-implantation studies B6CBAF1 mice, which were intraperitoneally inoculated with LPS (4–10 mg/kg), were used. Mice were also treated with vitamin E (4–10 mg/kg) before or after LPS injection. Embryos were obtained from the oviduct after each treatment.
Results: The LPS produces a decrease in the number of pre-implantational embryos in a concentration dependent manner. The LPS effect can be partially reversed or prevented by vitamin E. Preliminary results show that inflammatory cytokines are secreted by intraperitoneal macrophages in LPS treated mice.
Conclusion: Our results demonstrate the ability of vitamin E to avoid an inflammatory environment and to allow viability of embryos.