- 作者: Chiung-Chyi Shen; Hsueh-Meei Huang; Hsiu-Chung Ou; Huan-Lian Chen; Wen-Chi Chen; Kee-Ching Jeng
- 作者服務機構: Departments of Neurosurgery and Education and Research, Taichung Veterans General Hospital, Taichung, Taiwan, ROC; Burke Medical Research Institute, White Plains, N.Y.,USA
- 中文摘要: --
- 英文摘要: Nicotinamide (vitamin B3) reduces the infarct volume fol-lowing focal cerebral ischemia in rats; however, itsmechanism of action has not been reported. After cere-bral ischemia and/or reperfusion, reactive oxygen spe-cies (ROS) and reactive nitrogen species may be gener-ated by inflammatory cells through several cellular path-ways, which can lead to intracellular calcium influx andcell damage. Therefore, we investigated the mecha-nisms of action of nicotinamide in neuroprotection underconditions of hypoxia/reoxygenation. Results showedthat nicotinamide significantly protected rat primary cor-tical cells from hypoxia by reducing lactate dehydroge-nase release with 1 h of oxygen-glucose deprivation(OGD) stress. ROS production and calcium influx in neu-ronal cells during OGD were dose-dependently dimin-ished by up to 10 mM nicotinamide (p<0.01). This effectwas further examined with OGD/reoxygenation (H/R).Cells were stained with the fluorescent dye 4,6-diamidi-no-2-phenylindole (DAPI) or antibodies against anti-mi-crotubule-associated protein-2 and cleaved caspase-3.Apoptotic cells were studied using Western blotting ofcytochrome c and cleaved caspase-3. Results showedthat vitamin B3 reduced cell injury, caspase-3 cleavageand nuclear condensation (DAPI staining) in neuronalcells under H/R. In addition, nicotinamide diminished c-fos and zif268 immediate-early gene expressions follow-ing OGD. Taken together, these results indicate that theneuroprotective effect of nicotinamide might occurthrough these mechanisms in this in vitro ischemia/reperfusion model.
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- 英文關鍵字: --