Poly(ADP-ribose) polymerase-1 inhibition protects the brain against systemic inflammation.

Abstract

Poly(ADP-ribose) polymerase-1 (PARP-1) is involved in DNA repair, but its overactivation can induce cell death. Our aim was to investigate the role of PARP-1 in activation of programmed cell death processes in the brain during systemic inflammation. Our data indicated that lipopolysaccharide (1mg/kgb.w., i.p.)-evoked systemic inflammation enhanced PARP-1 activity in the mouse brain, leading to the lowering of beta-NAD(+) concentration, to translocation of apoptosis inducing factor from mitochondria to the nucleus, and to enhanced lipid peroxidation. Inhibitor of PARP-1, 3-aminobenzamide (30 mg/kgb.w., i.p.), protected the brain against prooxidative and cell death processes, suggesting involvement of PARP-1 in systemic inflammation-related processes in the brain.

• Authors: Grzegorz A Czapski, Magdalena Cakala, Barbara Gajkowska, Joanna B Strosznajder
• Journal: Neurochemistry international (Neurochem Int) Vol. 49 Issue 8 Pg. 751-5 (Dec 2006) ISSN: 0197-0186 [Print] England
• PMID: 16904242 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Benzamides
• Lipopolysaccharides
• Poly(ADP-ribose) Polymerase Inhibitors
• 3-aminobenzamide
• Parp1 protein, mouse
• Poly (ADP-Ribose) Polymerase-1

Topics

• Animals
• Benzamides (pharmacology)
• Brain (drug effects, enzymology, ultrastructure)
• Inflammation (enzymology)
• Lipopolysaccharides (pharmacology)
• Mice
• Microscopy, Electron
• Poly (ADP-Ribose) Polymerase-1
• Poly(ADP-ribose) Polymerase Inhibitors