鼠脑损伤后脑细胞外液中兴奋性氨基酸、葡萄糖与乳酸的含量变化及神经节苷酯GM1的保护作用
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摘要
目的:探讨损伤前后鼠脑细胞外液中兴奋性氨基酸、葡萄糖、乳酸的变化,并研究神经节苷酯GMI对大鼠脑损伤后的神经保护作用。
方法:以自由落体硬膜外撞击方法制作轻度和重度大鼠脑损伤模型,利用微透析技术收集不同组别脑损伤前后的细胞外液,检测兴奋性氨基酸、葡萄糖、乳酸的变化。
结果:对照组A组(假手术组)细胞外液中谷氨酸在伤后各时间段变化很小(P>0.05),基础水平为2.17±4-0.23μM。损伤组B组(损伤组)、C组(处理组)谷氨酸基础水平与对照组基本相同,伤后即迅速升高,各时间段波动明显,伤后15-30min时间段最高,B、C组谷氨酸分别为14.54±1.66和8.13±0.65μM(P<0.05),明显高于对照组,其后逐渐降低,至75-90min时间段接近对照组。
A组细胞外液中乳酸在伤后各时间段变化很小(P>0.05),基础水平为0.47±0.01mM。B、C组乳酸基础水平与A组基本相同,伤后即迅速升高,各时间段波动明显,伤后15-30min时间段最高,B、C组乳酸分别为0.83±0.07和0.75±0.06μM(P<0.05),明显高于对照组,其后逐渐降低,至75-90min时间段接近对照组。
A组细胞外液中葡萄糖在伤后各时间段变化很小(P>0.05),基础水平为0.42±0.03mM。B、C组葡萄糖基础水平与对照组基本相同,伤后即迅速降低,各时间段波动明显,伤后15-30min时间段达低谷,B、C组葡萄糖分别为0.27±0.02和0.33±0.02mM(P<0.05),明显低于对照组,其后逐渐回升,至75-90min时间段接近对照组。
结论:脑损伤后早期,透析液中兴奋性氨基酸持续升高,有一个明显的峰值,证实了损伤引起的神经损害与兴奋性氨基酸有关,同时,为临床治疗、给药的时间窗的把握提供了理论根据。
脑损伤后,早期使用GM1治疗,兴奋性氨基酸的曲线峰值明显下降,提示GM1对兴奋性氨基酸引起的脑损伤有明确的保护作用。为进一步的临床运用提供参考依据。
脑损伤后,观察到早期使用GM1治疗,可以减轻脑组织中乳酸的堆积,增加葡萄糖含量,从而改善能量代谢,增强神经元细胞的存活,这为探索GM1在脑损伤后的神经保护提供了新的途径。
Objective: To study the change of excitability amino acid(EAA), glucose, lactic acid in mouse brain extracellular fluid(ECF), and to study the protective function of gangliosides GM1 on mouse brain.
Methods: The change of Glutamic acid(Glu) in ECF of the control group A (sham-operation group) is not significant after injury(P> 0.05). In injury group B group (injury group), C group (treatment group), the basic level of Glu is same as that of control group A , Glu rised rapidly after injury, the undulation of Glu is obvious, and is highest during 15-30min after injury, Glu of group B and group C were 14.54±1.66 and 8.13±0.65μM respectively (P < 0.05), were higher than the control group obviously(P < 0.05), then reduced gradually to the level of group A after 75-90min.
The change of lactic acid in ECF of the control group A (sham-operation group) is not significant after mjury(P> 0.05). In injury group B group (injury group), C group (treatment group), the basic level of lactic acid is same as that of control group A , lactic acid ascended rapidly after injury, the undulation of lactic acid is obvious, and is highest during 15-30min after injury, lactic acid of group B and group C were 0.83±0.07 and 0.75±0.06 u M respectively (P < 0.05), were higher than the control group obviously(P < 0.05), then reduced gradually to the level of group A after 75-90min .
The change of glucose in ECF of the control group A (sham-operation group) is not significant after injury(P> 0.05). In injury group B group (injury group), C group (treatment group), the basic level of glucose is same as that of control group A , glucose descended rapidly after injury, the undulation of glucose is obvious, and is highest during 15-30min injury, glucose of group B and group C were 0.27±0.02 and 0.33±0.02mM respectively (P < 0.05), were higher than the control group obviously(P < 0.05), then ascended gradually to the level of group A after 75-90min.
Conclusion:, In the dialyzate, excitability amino acid ascended continually in the early after injury, then to a peak value, this confirmed the relationship between the brain injury and excitability amino acid .Simultaneously, it was the theory basis for the clinical treatment, and identified the medicine time window.
After the early use of GM1, peak value of the excitability amino acid droped obviously, hinted that GM1 have the explicit protective function on the brain injury which caused by the excitability amino acid. Provided the reference for the further clinical utilization.
After the brain injury, the early use of GM1 reduced the stack of lactic acid in brain tissue , and increased the content of glucose, thus improved energy metabolism , and were good for neuron cell, which may afford useful clues for the treatment of brain injury with GM1
方法:以自由落体硬膜外撞击方法制作轻度和重度大鼠脑损伤模型,利用微透析技术收集不同组别脑损伤前后的细胞外液,检测兴奋性氨基酸、葡萄糖、乳酸的变化。
结果:对照组A组(假手术组)细胞外液中谷氨酸在伤后各时间段变化很小(P>0.05),基础水平为2.17±4-0.23μM。损伤组B组(损伤组)、C组(处理组)谷氨酸基础水平与对照组基本相同,伤后即迅速升高,各时间段波动明显,伤后15-30min时间段最高,B、C组谷氨酸分别为14.54±1.66和8.13±0.65μM(P<0.05),明显高于对照组,其后逐渐降低,至75-90min时间段接近对照组。
A组细胞外液中乳酸在伤后各时间段变化很小(P>0.05),基础水平为0.47±0.01mM。B、C组乳酸基础水平与A组基本相同,伤后即迅速升高,各时间段波动明显,伤后15-30min时间段最高,B、C组乳酸分别为0.83±0.07和0.75±0.06μM(P<0.05),明显高于对照组,其后逐渐降低,至75-90min时间段接近对照组。
A组细胞外液中葡萄糖在伤后各时间段变化很小(P>0.05),基础水平为0.42±0.03mM。B、C组葡萄糖基础水平与对照组基本相同,伤后即迅速降低,各时间段波动明显,伤后15-30min时间段达低谷,B、C组葡萄糖分别为0.27±0.02和0.33±0.02mM(P<0.05),明显低于对照组,其后逐渐回升,至75-90min时间段接近对照组。
结论:脑损伤后早期,透析液中兴奋性氨基酸持续升高,有一个明显的峰值,证实了损伤引起的神经损害与兴奋性氨基酸有关,同时,为临床治疗、给药的时间窗的把握提供了理论根据。
脑损伤后,早期使用GM1治疗,兴奋性氨基酸的曲线峰值明显下降,提示GM1对兴奋性氨基酸引起的脑损伤有明确的保护作用。为进一步的临床运用提供参考依据。
脑损伤后,观察到早期使用GM1治疗,可以减轻脑组织中乳酸的堆积,增加葡萄糖含量,从而改善能量代谢,增强神经元细胞的存活,这为探索GM1在脑损伤后的神经保护提供了新的途径。
Objective: To study the change of excitability amino acid(EAA), glucose, lactic acid in mouse brain extracellular fluid(ECF), and to study the protective function of gangliosides GM1 on mouse brain.
Methods: The change of Glutamic acid(Glu) in ECF of the control group A (sham-operation group) is not significant after injury(P> 0.05). In injury group B group (injury group), C group (treatment group), the basic level of Glu is same as that of control group A , Glu rised rapidly after injury, the undulation of Glu is obvious, and is highest during 15-30min after injury, Glu of group B and group C were 14.54±1.66 and 8.13±0.65μM respectively (P < 0.05), were higher than the control group obviously(P < 0.05), then reduced gradually to the level of group A after 75-90min.
The change of lactic acid in ECF of the control group A (sham-operation group) is not significant after mjury(P> 0.05). In injury group B group (injury group), C group (treatment group), the basic level of lactic acid is same as that of control group A , lactic acid ascended rapidly after injury, the undulation of lactic acid is obvious, and is highest during 15-30min after injury, lactic acid of group B and group C were 0.83±0.07 and 0.75±0.06 u M respectively (P < 0.05), were higher than the control group obviously(P < 0.05), then reduced gradually to the level of group A after 75-90min .
The change of glucose in ECF of the control group A (sham-operation group) is not significant after injury(P> 0.05). In injury group B group (injury group), C group (treatment group), the basic level of glucose is same as that of control group A , glucose descended rapidly after injury, the undulation of glucose is obvious, and is highest during 15-30min injury, glucose of group B and group C were 0.27±0.02 and 0.33±0.02mM respectively (P < 0.05), were higher than the control group obviously(P < 0.05), then ascended gradually to the level of group A after 75-90min.
Conclusion:, In the dialyzate, excitability amino acid ascended continually in the early after injury, then to a peak value, this confirmed the relationship between the brain injury and excitability amino acid .Simultaneously, it was the theory basis for the clinical treatment, and identified the medicine time window.
After the early use of GM1, peak value of the excitability amino acid droped obviously, hinted that GM1 have the explicit protective function on the brain injury which caused by the excitability amino acid. Provided the reference for the further clinical utilization.
After the brain injury, the early use of GM1 reduced the stack of lactic acid in brain tissue , and increased the content of glucose, thus improved energy metabolism , and were good for neuron cell, which may afford useful clues for the treatment of brain injury with GM1
引文
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[35] Goodman JC, Valadka AB, Gopinath SP,et al.Extracellular lactate and glucose alterations in the brain after head injury measured by microdialysis. Crit Care Med,1999, 27(9): 1965-73.
[36] Marion DW, Puccio A, Wisniewski SR,et al.Effect of hyperventilation on extracellular concentrations of glutamate, lactate, pyruvate, and local cerebral blood flow in patients with severe traumatic brain injury. Crit Care Med, 2002,30(12):2619-2625.
[37] Lee GJ, Park JH, Park HK.Microdialysis applications in neuroscience.Neurol Res. 2008 Sep;30(7):661-8. Epub 2008 Jul 15.
[38] Uehara T, Sumiyoshi T, Itoh H, Kurata K.Lactate production and neurotransmitters; evidence from microdialysis studies. Pharmacol Biochem Behav. 2008 Aug;90(2):273-81. Epub 2008 Apr 8. Review.
[39] Microdialysis sampling method for evaluation of binding kinetics of small molecules to macromolecules.Anal Chem. 2008 Apr 15;80(8):2993-9. Epub 2008 Mar 21.
[40] van der Zeyden M, Oldenziel WH, Rea K, Cremers TI, Westerink BH.Microdialysis of GABA and glutamate: analysis, interpretation and comparison with microsensors. Pharmacol Biochem Behav. 2008 Aug;90 (2):135-47. Epub 2007 Sep 14. Review.
[41] Zhou SN, Ouyang G, Pawliszyn J.Comparison of microdialysis with solid-phase microextraction for in vitro and in vivo studies.J Chromatogr A. 2008 Jul 4; 1196-1197:46-56. Epub 2008 Feb 26.
[1] Matsushita Y et al. Real-time monitoring of glutamate following fluid percussion brain injury with hypoxia in the rat. J Neuronranma,2000,17(2):143-153
[2] Roberts WA, Eaton SA, Salt TE. Excitatory amino acid receptors mediate synaptic responses to visual stimuli in superior colliculus neurones of the rat.Neurosci Lett 1991 Aug 19;129(2):161-4
[3] Lindholm D. Models to study the role of neurotrophic factors in neurodegeneration. J Neural Transm Suppl 1997;49:33-42
[4] Hick D et al. Growth factors and gangliosides as neuroprotective agents in excitotoxicity and ischemia. Gen Pharmacol, 1998;Mar;30(3):265
[5] Skaper SD, Leon A. Monosialogangliosides, neuroprotection, and neuronal repair processes. J Neurotrauma 1992 May;9 Suppl 2:S507-16
[6] Itoh M, Fukumoto S, Iwamoto T, et al. Specificity of carbohydrate structures of gangliosides in the activity to regenerate the rat axotomized hypoglossal nerve. Glycobiology, 2001 ;Feb;11(2): 125
[7] Willison HJ, Almemar A, Veitch J et al. Acute ataxic neuropathy with cross-reactive antibodies to GD1b and GD3 gangliosides, Neurology 1994 Dec;44(12):2395-7
[8] Nobile-Orazio E, Carpo M, Scarlato G Gangliosides. Their role in clinical neurology. Drugs 1994 Apr;47(4):576-85
[9] Schneider JS, Roeltgen DP, Mancall EL et al. Parkinson's disease: improved function with GM1 ganglioside treatment in a randomized placebo-controlled study. Neurology 1998 Jun;50(6): 1630-6
[10] Favaron M, et al. Natural and semisynthetic sphingolipids protect neurons in culture from glutamate induced toxicity in :Biggo G, et al eds. Excitatory amino acids and brain ischemia. Oxford, Pergamon press, 1990;93-102
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[15] Wu G, Lu ZH, Ledeen RW. Induced and spontaneous neuritogenesis are associated with enhanced expression of ganglioside GM1 in the nuclear membrane. J Neurosci 1995 May;15(5 Pt 2):3739-46
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[1] Matsushita Y et al. Real-time monitoring of glutamate following fluid percussion brain injury with hypoxia in the rat. J Neuronranma,2000,17(2):143-153
[2] Roberts WA, Eaton SA, Salt TE. Excitatory amino acid receptors mediate synaptic responses to visual stimuli in superior colliculus neurones of the rat.Neurosci Lett 1991 Aug 19;129(2):161-4
[3] Lindholm D. Models to study the role of neurotrophic factors in neurodegeneration. J Neural Transm Suppl 1997;49:33-42
[4] Hick D et al. Growth factors and gangliosides as neuroprotective agents in excitotoxicity and ischemia. Gen Pharmacol, 1998;Mar;30(3):265
[5] Skaper SD, Leon A. Monosialogangliosides, neuroprotection, and neuronal repair processes. J Neurotrauma 1992 May;9 Suppl 2:S507-16
[6] Itoh M, Fukumoto S, Iwamoto T, et al. Specificity of carbohydrate structures of gangliosides in the activity to regenerate the rat axotomized hypoglossal nerve. Glycobiology, 2001 ;Feb;11(2): 125
[7] Willison HJ, Almemar A, Veitch J et al. Acute ataxic neuropathy with cross-reactive antibodies to GD1b and GD3 gangliosides, Neurology 1994 Dec;44(12):2395-7
[8] Nobile-Orazio E, Carpo M, Scarlato G Gangliosides. Their role in clinical neurology. Drugs 1994 Apr;47(4):576-85
[9] Schneider JS, Roeltgen DP, Mancall EL et al. Parkinson's disease: improved function with GM1 ganglioside treatment in a randomized placebo-controlled study. Neurology 1998 Jun;50(6): 1630-6
[10] Favaron M, et al. Natural and semisynthetic sphingolipids protect neurons in culture from glutamate induced toxicity in :Biggo G, et al eds. Excitatory amino acids and brain ischemia. Oxford, Pergamon press, 1990;93-102
[11] Skaper SD, Leon A, Facci L. Ganglioside GM1 prevents death induced by excessive excitatory neurotransmission in cultured hippocampal pyramidal neurons. Neurosci Lett 1991 May 13;126(1):98-101
[12] Frontczak-Baniewicz M, Gadamski R, Barskov I et al. Beneficial effects of GM1 ganglioside on photochemically-induced microvascular injury in cerebral cortex and hypophysis in rat. Exp Toxicol Pathol 2000 May;52(2):111-8
[13] Ledeen RW. Biology of gangliosides: neuritogenic and neuronotrophic propertie, J Neurosci Res 1984;12(2-3):147-59
[14] Cunha GM, Moraes RA, Moraes GA et al. Nerve growth factor, ganglioside and vitamin E reverse glutamate cytotoxicity in hippocampal cells. Eur J Pharmacol 1999 Feb 12;367(1):107-12
[15] Wu G, Lu ZH, Ledeen RW. Induced and spontaneous neuritogenesis are associated with enhanced expression of ganglioside GM1 in the nuclear membrane. J Neurosci 1995 May;15(5 Pt 2):3739-46
[16] Schneider JS, Kean A, DiStefano L. GM1 ganglioside rescues substantia nigra pars compacta neurons and increases dopamine synthesis in residual nigrostriatal dopaminergic neurons in MPTP-treated mice. J Neurosci Res 1995 Sepl;42(1):117-23
[17] Duchemin AM, et al, GM1 increase the content and mRNA NGF in brain of aged rats. Neurorreport, 1997;8 (17):3823-3827
[18] Rosenberg PA, Azenman E. Hundred-fold increase in neuronal vulnerability to glutamate toxicity in astrocyte-pooreultures of rat cerebral cortex. Neuro lett,1998,103(2):162
[19] Mahadik SP, Vilim F, Korenovsky et al. GM1 ganglioside protects nucleus basalis from excitotoxin damage: reduced cortical cholinergic losses and animal mortality. J Neurosci Res 1988 Aug;20(4):479-83
[20] Tanaka K, et al. Effect of the ganglioside GM1 on cerebral metabolism,microcirculation, recovery kinetics of EcoG and histology, during the recovery period following focal ischemia in cats. Stroke, 1986; 17:1170
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