Certainly, pharmacologically inhibiting GSK-3β confer the possible therapeutic effects against renal injury in vivo in the rat model of ischemia [15] and the murine models of endotoxemia [20] and pharmacological stimulation, including nonsteroidal anti-inflammatory drug diclofenac and mercuric chloride [21,22]. This evidence concerns the gene GSK3B and serum lipopolysaccharide activity.