Yang Jun, Klaidman Lori K, Nalbandian Artak, Oliver Jasmine, Chang Mei L, Chan Pak H, Adams James D
Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, 1985 Zonal Avenue, Los Angeles, CA 90089-9121, USA.
Neurosci Lett. 2002 Nov 22;333(2):91-4. doi: 10.1016/s0304-3940(02)01005-4.
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.
本研究考察了烟酰胺对氯胺酮预处理大鼠缺血再灌注后三磷酸腺苷(ATP)、烟酰胺腺嘌呤(NAD)水平及聚(二磷酸腺苷 - 核糖)(聚(ADP - 核糖))聚合酶活性的影响。在缺血期结束时给予烟酰胺。烟酰胺可防止再灌注6小时和24小时时ATP和NAD的消耗。已知烟酰胺在早期时间点会抑制聚(ADP - 核糖)聚合酶,但发现在再灌注24小时时会增加聚(ADP - 核糖)聚合酶活性。似乎烟酰胺可在再灌注期间帮助维持细胞能量代谢,从而保护细胞免受坏死和凋亡机制的影响。