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目的 :研究果糖二磷酸钠镁 (FDPM)对缺血突触体乳酸含量及ATP酶活性的影响 ,以探讨其脑保护作用机制。方法 :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 ,分别加 1.3mmol·L- 1硫酸镁 ,4 .0mmol·L- 11,6 二磷酸果糖 (FDP)及 1.3mmol·L- 1果糖二磷酸钠镁共培养 6 0min ,测定突触体乳酸含量及Na+ K+ATP酶和Ca2 + Mg2 +ATP酶活性。结果 :FDPM可明显降低缺血突触体乳酸含量 ,升高Na+ K+ATP酶和Ca2 + Mg2 +ATP酶活性(P <0 .0 5 ) ,其作用强于FDP的作用。结论 :FDPM保护脑缺血的作用机制可能与其改善脑缺血后能量代谢 ,减轻脑组织酸中毒状态有关
Objective: To study the effect of sodium magnesium fructose diphosphate (FDPM) on the content of lactic acid and the activity of ATPase in ischemic synaptosome in order to explore its mechanism of cerebral protection. Methods: The normal rat brain synaptosomes were prepared and the model of ischemic synaptosomes was established by oxygen-glucose deprivation. The rats were treated with 1.3 mmol·L -1 magnesium sulfate, 4.0 mmol·L -1 fructose diphosphate (FDP) and 1.3 mmol·L-1 sodium magnesium fructose diphosphate co-cultured 60min, measured synaptosome content of lactic acid and Na + K + ATPase and Ca2 + Mg2 + ATPase activity. Results: FDPM could significantly decrease the content of lactic acid in ischemic synaptosome, increase the activity of Na + K + ATPase and Ca2 + Mg2 + ATPase (P <0.05), which is stronger than that of FDP. Conclusion: The mechanism of FDPM in protecting cerebral ischemia may be related to improving energy metabolism after cerebral ischemia and ameliorating acidosis in brain tissue