LAUSR

Brilliant blue G or Coomassie blue is a purinergic P2X7 receptor antagonist. In this study, the effect of brilliant blue G on serum oxidative stress and brain and liver tissue damage was studied in rats with lipopolysaccharide (LPS)-induced systemic inflammation. Rats were treated with intraperitoneal (i.p.) injection of Escherichia coli LPS (300 μg/kg) alone or together with brilliant blue G at 5 or 10 mg/kg and euthanized 4 h thereafter. Serum malondialdehyde, nitric oxide, paraoxonase 1 (PON-1) activity, cholinesterase activity, and glucose were determined. In addition, brain and liver histopathology, and caspase-3 and glial fibrillary acidic protein (GFAP) immunostaining were done. Results indicated that LPS produced a significant elevation in serum malondialdehyde and nitric oxide concentrations along with markedly decreased PON-1 activity and glucose. LPS caused neuronal degeneration in the cerebral cortex and hippocampus, increased caspase-3, and decreased GFAP immunostaining in the cerebral cortex. Vacuolar degeneration and inflammation were observed in the liver of LPS-treated rats. The administration of brilliant blue G decreased serum malondialdehyde by 34.5–35.2% and nitric oxide concentrations by 27.4–35.6%, respectively, while increasing PON-1 activity by 46.3–86.7% and serum glucose level by 24.8%. Moreover, brilliant blue G inhibited serum cholinesterase activity by 38.1–42% compared with the LPS control group. Brilliant blue G attenuated the neuronal degeneration, the increase in caspase-3 activity, and the decrease in GFAP-positive astrocytes produced by LPS. It also decreased hepatic cellular infiltration and congestion. These results indicate that brilliant blue G is able to ameliorate the brain and liver tissue damage during LPS-induced systemic inflammation and suggest a potential therapeutic use of brilliant blue G to prevent organ damage during systemic endotoxemia.