Zeng Fan-xin, Dong Zhi, Zhou Qi-xin
Department of Pharmacology and Toxicology, Chongqing Pharmaceutical Research Institute, Chongqing 400061, China.
Yao Xue Xue Bao. 2003 May;38(5):325-7.
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.
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.
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.
SMFD may protect neurons from ischemic injury by preventing intracellular Ca2+ overload and inhibiting the activity of nitric oxide synthase.
研究果糖二磷酸钠镁（SMFD）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SMFD对脑缺血的保护机制。
采用相分离法制备正常大鼠脑突触体，通过无糖缺氧培养建立缺血突触体模型。将突触体分别与SMFD（1.3 mmol·L-1）或1,6-二磷酸果糖（FDP，4.0 mmol·L-1）共同孵育60分钟后，分别检测突触体内游离钙浓度及一氧化氮合酶活性。
SMFD可降低缺血突触体的游离钙浓度，并降低一氧化氮合酶（NOS）的活性。其作用比FDP更强。
SMFD可能通过防止细胞内Ca2+超载及抑制一氧化氮合酶活性来保护神经元免受缺血损伤。
