Genovese Tiziana, Mazzon Emanuela, Mariotto Sofia, Menegazzi Marta, Cardali Salvatore, Conti Alfredo, Suzuki Hisanori, Bramanti Placido, Cuzzocrea Salvatore
Institute of Pharmacology, University of Messina, Italy.
J Neurosurg Spine. 2006 Feb;4(2):145-53. doi: 10.3171/spi.2006.4.2.145.
A traumatic spinal cord injury (SCI) immediately induces primary damage, and this is followed by secondary damage characterized by a series of events among which is a progressive extension of cell death within the damaged tissue. In this study, the authors investigated the role of inducible nitric oxide synthase (iNOS) in an experimental model of SCI in mice.
In wild-type (iNOS+/+) mice, SCI rapidly induced an inflammatory response as shown by nitrotyrosine formation, activation of the nuclear enzyme poly(adenosine diphosphate-ribose) polymerase (PARP), neutrophil infiltration, and spinal cord tissue histopathological changes, indicating the involvement of iNOS-derived massive amounts of NO in SCI.
Genetic inhibition of iNOS, however, resulted in a significant reduction in secondary damage, and this therapeutic efficacy was associated with the prevention of an SCI-induced drop in neuronal and endothelial NOS activity.
创伤性脊髓损伤（SCI）会立即引发原发性损伤，随后是继发性损伤，其特征是一系列事件，其中包括受损组织内细胞死亡的逐渐扩展。在本研究中，作者研究了诱导型一氧化氮合酶（iNOS）在小鼠SCI实验模型中的作用。
在野生型（iNOS+/+）小鼠中，SCI迅速引发炎症反应，表现为硝基酪氨酸形成、核酶聚（腺苷二磷酸-核糖）聚合酶（PARP）激活、中性粒细胞浸润和脊髓组织组织病理学变化，表明iNOS衍生的大量NO参与了SCI。
然而，iNOS的基因抑制导致继发性损伤显著减少，这种治疗效果与预防SCI诱导的神经元和内皮型NOS活性下降有关。
