Fontella Fernanda Urruth, Cimarosti Helena, Crema Leonardo Machado, Thomazi Ana Paula, Leite Marina Concli, Salbego Christianne, Gonçalves Carlos Alberto Saraiva, Wofchuk Susana, Dalmaz Carla, Netto Carlos Alexandre
PPG-Fisiologia e Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, UFRGS, Rua Ramiro Barcelos, 2600 anexo, 90035-003 Porto Alegre, RS, Brazil.
Brain Res Bull. 2005 May 15;65(5):443-50. doi: 10.1016/j.brainresbull.2005.02.026.
Several studies have shown that high corticosteroid hormone levels increase neuronal vulnerability. Here we evaluate the consequences of in vivo acute or repeated restraint stress on cellular viability in rat hippocampal slices suffering an in vitro model of ischemia. Cellular injury was quantified by measuring lactate dehydrogenase (LDH) and neuron-specific enolase released into the medium. Acute stress did not affect cellular death when oxygen and glucose deprivation (OGD) was applied both immediately or 24h after restraint. The exposure to OGD, followed by reoxygenation, resulted in increased LDH in the medium. Repeated stress potentiated the effect of OGD both, on LDH and neuron-specific enolase released to the medium. There was no effect of repeated stress on the release of S100B, an astrocytic protein. Additionally, no effect of repeated stress was observed on glutamate uptake by the tissue. These results suggest that repeated stress increases the vulnerability of hippocampal cells to an in vitro model of ischemia, potentiating cellular damage, and that the cells damaged by the exposure to repeated stress+OGD are mostly neurons. The uptake of glutamate was not observed to participate in the mechanisms responsible for rendering the neurons more susceptible to ischemic damage after repeated stress.
多项研究表明，高皮质类固醇激素水平会增加神经元的易损性。在此，我们评估了体内急性或反复束缚应激对遭受体外缺血模型的大鼠海马切片细胞活力的影响。通过测量释放到培养基中的乳酸脱氢酶（LDH）和神经元特异性烯醇化酶来量化细胞损伤。当在束缚后立即或24小时施加氧和葡萄糖剥夺（OGD）时，急性应激不影响细胞死亡。暴露于OGD后再进行复氧，会导致培养基中LDH增加。反复应激增强了OGD对释放到培养基中的LDH和神经元特异性烯醇化酶的影响。反复应激对星形胶质细胞蛋白S100B的释放没有影响。此外，未观察到反复应激对组织摄取谷氨酸有影响。这些结果表明，反复应激会增加海马细胞对体外缺血模型的易损性，加剧细胞损伤，并且暴露于反复应激+OGD后受损的细胞主要是神经元。未观察到谷氨酸摄取参与反复应激后使神经元更易受缺血损伤的机制。
