果糖二磷酸钠镁对缺血突触体游离钙浓度及一氧化氮合酶活性的影响

目的研究果糖二磷酸钠镁对缺血突触体游离钙浓度及一氧化氮合酶活性的影响,以探讨其保护脑缺血的作用机制。方法以相分离法制备正常大鼠脑突触体,氧糖剥夺培养建立缺血突触体模型,加入1.3 mmol·L^-1 SMFD,4.0 mmol·L^-1 FDP与之培养60 min后,测定突触体内游离钙浓度和一氧化氮合酶活性。结果1.3 mmol·L^-1 SMFD可明显降低缺血突触体内游离钙浓度,降低一氧化氮合酶活性,其作用强于4.0 mmol·L^-1 FDP。结论SMFD保护脑缺血的作用机制可能与其阻止脑缺血后细胞内钙超载,抑制一氧化氮合酶活性有关。

Effects of sodium magnesium fructose diphosphate on free calcium concentration and nitric oxide synthase activity of ischemic synaptosome

AIM: To study the effects of sodium magnesium fructose diphosphate (SMFD) on free calcium concentration and nitric oxide synthase activity of ischemic synaptosome, so as to explore the protective mechanisms of SMFD on cerebral ischemia. METHODS: The synaptosomes from normal rat brain were prepared by phase partition and cultured with oxygen-glucose deprivation to establish ischemic synaptosome model. The intrasynaptosomal free calcium concentration and nitric oxide synthase activity were detected separately after the synaptosomes were co-incubated with SMFD (1.3 mmol.L-1) or fructose-1, 6-diphosphate (FDP, 4.0 mmol.L-1) for 60 min. RESULTS: SMFD decreased the free calcium concentration and reduced the activity of nitric oxide synthase (NOS) of ischemic synaptosomes. Its effects were more powerful than those of FDP. CONCLUSION: SMFD may protect neurons from ischemic injury by preventing intracellular Ca2+ overload and inhibiting the activity of nitric oxide synthase.