摘要
目的:研究果糖二磷酸钠镁对缺血突触体乳酸含量、胞内游离钙浓度及ATP酶与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1.3mmol/L的果糖二磷酸钠镁,4.0mmol/L的1,6-二磷酸果糖与之培养60min后,测定突触体乳酸含量、胞内游离钙浓度及ATP酶与一氧化氮合酶活性。结果:氧糖剥夺培养后使突触体乳酸浓度显著增加,从(0.201±0.014)mmol/L增加到(0.282±0.018)mmol/L(F=11.4178,P<0.01),突触体内游离钙浓度也显著增加(P<0.01);一氧化氮合酶活性显著增高,从(13.669±1.084)nkat增加至(44.142±1.167)nkat(F=44.8472,P<0.01);而ATP酶活性显著降低(P<0.01)。加入1.3mmol/L果糖二磷酸钠镁与之共孵,可使缺血突触体乳酸含量降至(0.204±0.016)mmol/L(F=10.4371,P<0.01);静息状态和除极化状态突触体内游离钙浓度分别降低(P<0.01),一氧化氮合酶活性降低为(18.654±1.317)nkat(F=28.0423,P<0.01),而Na+-K+ATP酶和Ca2+-Mg2+ATP酶活性升高(P<0.01)。果糖二磷酸钠镁的作用强于4.0mmol/L的1,6-二磷酸果糖(P<0.01)。结论:果糖二磷酸钠镁保护脑缺血的作用机制可能与其阻止改善脑缺血后脑组织能量代谢,减轻组织酸中毒,阻止细胞内钙超载及抑?
AIM:To study the effects of sodium magnesium fructose diphosphate(SMFD) on lactate concentration, introcellular free calcium concentration, ATPase and nitric oxide synthase(NOS) activity of ischemic synaptosome, so as to explore the protective mechanism of SMFD on cerebral ishcemia. METHODS:The synaptosome of normal rat was prepared with phase partition and cultured with oxygen glucose deprived to establish ischemic synaptosome model.The lactate concentration, intracellular free calcium concentration,ATPase and NOS activity were detected respectively after the synaptosome was cocultured with SMFD(1.3 mmol/L) and fructose 1,6 diphos phate(FDP,4.0 mmol/L) for 60 minutes. RESULTS:Culture deprived with oxygen glucose significantly increased lactate concentration of synaptosome[from(0.201±0.014) mmol/L to(0.282±0.018) mmol/L,F=11.417 8,P< 0.01],as well as intracellular free calcium concentration,and NOS activity was significantly increased from(13.669±1.084)nkat to(44.142±1.167)nkat(P< 0.01,F=44.847 2),while the activity of ATPase was decreased significantly(P< 0.01).Preincubation with SMFD significantly reduced lactate concentration of ischemic synaptosome to(0.204±0.016) mmol/L(F=10.437 1,P< 0.01),and decreased introcellular free calcium concentration under resting and depolarizing states respectively(P< 0.01),and reduced NOS activity to(18.654±1.317) nkat(F=28.042 3,P< 0.01),and increased the activities of Na+ K+ATPase and Ca2+ Mg2+ATPase(P< 0.01).Effects of SMFD were more powerful than those of FDP(4.0 mmol/L)(P< 0.01). CONCLUSION:SMFD may protect neurons from ischemic injury by improving the energy metablism,mitigating acidosis state of brain tissue,preventing intracellular Ca2+overload and inhibiting the activity of nitric oxide synthase after ischemia.
出处
《中国临床康复》
CSCD
2004年第19期3798-3799,共2页
Chinese Journal of Clinical Rehabilitation
