In addition, the current result agrees with the previous study that, by reducing the degradation of IκBα, PPAR-γ agonist repressed NF-κB in the lung and reduced lung injury at 18 hours after CLP [16], suggesting that this protective mechanism mediated by PPAR-γ may be applicable to other organ injuries in sepsis. This evidence concerns the gene NFKB1 and Sepsis.