Cimarosti H, Rodnight R, Tavares A, Paiva R, Valentim L, Rocha E, Salbego C
Departamento de BioquImica, Instituto de Ciências Básicas da Saúde, UFRGS, 90035-003, Porto Alegre, Brazil.
Neurosci Lett. 2001 Nov 23;315(1-2):33-6. doi: 10.1016/s0304-3940(01)02310-2.
Brain ischemia results in cellular degeneration and loss of function. Here we investigated the neuroprotective effect of lithium in an in vitro model of ischemia. Organotypic hippocampal slice cultures were exposed to oxygen and glucose deprivation. Cellular death was quantified by measuring uptake of propidium iodide (PI). Lithium chloride (0.2-1.2 mM) was added to the medium before, during and after lesion induction. A decrease in incorporation of PI was observed, indicating a neuroprotective effect in all doses tested. We also studied the effect of lithium on the phosphorylation of HSP27, a heat shock protein involved in cellular protection in its dephosphorylated state. In the lesioned hippocampus, 0.4 mM lithium chloride decreased the proportion of phosphorylated HSP27 to total HSP27. These results suggest that lithium may be useful in the treatment of brain ischemia.
脑缺血会导致细胞变性和功能丧失。在此,我们在体外缺血模型中研究了锂的神经保护作用。将器官型海马切片培养物暴露于氧和葡萄糖剥夺环境中。通过测量碘化丙啶(PI)摄取量来定量细胞死亡。在损伤诱导前、期间和之后,向培养基中添加氯化锂(0.2 - 1.2 mM)。观察到PI掺入量减少,表明在所有测试剂量下均有神经保护作用。我们还研究了锂对HSP27磷酸化的影响,HSP27是一种热休克蛋白,在其去磷酸化状态下参与细胞保护。在受损海马中,0.4 mM氯化锂降低了磷酸化HSP27与总HSP27的比例。这些结果表明锂可能对治疗脑缺血有用。