TLR4 activation triggers the biosynthesis of different inflammation mediators, such as tumor necrosis factor (TNF) and interleukins (IL-1, IL-6, IL-8, IL-18), which stimulate the release of prostaglandins and leukotrienes [11,18], eventually leading to inflammation and septic shock, which are the most significant features of endotoxemia [21,22]. This evidence concerns the gene TNF and serum lipopolysaccharide activity.