The effects of nicotinamide on energy metabolism following transient focal cerebral ischemia in Wistar rats

Neurosci Lett. 2002 Nov 22;333(2):91-4. doi: 10.1016/s0304-3940(02)01005-4.

Abstract

This study examined the effects of nicotinamide on adenosine triphosphate (ATP) and nicotinamide adenine (NAD) levels and poly(adenosine diphosphate-ribose) (poly(ADP-ribose)) polymerase activity following ischemia and reperfusion in ketamine pretreated rats. Nicotinamide was administered at the end of the ischemic period. Nicotinamide protected against the depletion of ATP and NAD at 6 and 24 h of reperfusion. Nicotinamide is known to inhibit poly(ADP-ribose) polymerase at early time points, but was found to increase poly(ADP-ribose) polymerase activity at 24 h of reperfusion. It appears that nicotinamide can help maintain cellular energetics during reperfusion, thereby protecting cells from necrotic and apoptotic mechanisms.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenosine Triphosphate / analysis
  • Animals
  • Brain / drug effects*
  • Brain / metabolism
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / metabolism
  • Corpus Striatum / drug effects
  • Corpus Striatum / metabolism
  • Energy Metabolism / drug effects*
  • Ischemic Attack, Transient / metabolism*
  • Male
  • NAD / analysis
  • Neuroprotective Agents / pharmacology*
  • Niacinamide / pharmacology*
  • Poly(ADP-ribose) Polymerases / analysis
  • Rats
  • Rats, Wistar
  • Reperfusion
  • Time Factors

Substances

  • Neuroprotective Agents
  • NAD
  • Niacinamide
  • Adenosine Triphosphate
  • Poly(ADP-ribose) Polymerases