Based on an endotoxemia model and in conjunction with proteomics, Western blot, real-time PCR, enzyme activity and survival evaluations, the present study revealed that augmented polyubiquitination, enhanced proteasomal activities and recycling of ubiquitin through sustained de-ubiquitination in RVLM play a vital role during brain death. The gene discussed is UBB; the disease is serum lipopolysaccharide activity.