Charriaut-Marlangue C, Margaill I, Borrega F, Plotkine M, Ben-Ari Y
Université R. Descartes, INSERM U29, Paris, France.
Eur J Pharmacol. 1996 Aug 29;310(2-3):137-40. doi: 10.1016/0014-2999(96)00385-8.
During cerebral ischemia, nitric oxide (NO) production via stimulation of NO synthase, is likely one of the major events leading to neuronal death. Recently, we have demonstrated that after reversible focal ischemia, apoptosis was implicated in the penumbra whereas necrosis was prominent in the ischemic core. We have now examined the effect of a non-specific inhibitor of NO synthase, NG-nitro-L-arginine methyl ester (L-NAME, 3 ing kg-1 i.p., 5 min and 3 h after the onset of ischemia), on the progress of apoptotic and necrotic nuclei following transient focal cerebral ischemia, using DNA electrophoresis and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick-end labeling (TUNEL assay). Our results indicated that L-NAME prevented the loss of necrotic, but not apoptotic cells.
在脑缺血期间，通过刺激一氧化氮合酶产生一氧化氮（NO）可能是导致神经元死亡的主要事件之一。最近，我们已经证明，在可逆性局灶性缺血后，凋亡发生在半暗带，而坏死在缺血核心区较为突出。我们现在使用DNA电泳和末端脱氧核苷酸转移酶（TdT）介导的dUTP生物素缺口末端标记（TUNEL法），研究了一氧化氮合酶非特异性抑制剂NG-硝基-L-精氨酸甲酯（L-NAME，缺血发作后5分钟和3小时腹腔注射3毫克/千克）对短暂性局灶性脑缺血后凋亡和坏死细胞核进展的影响。我们的结果表明，L-NAME可防止坏死细胞的丢失，但不能防止凋亡细胞的丢失。
