L-pyroglutamic acid protects rat cortical neurons against sodium glutamate-induced injury.

X Q Xiao, G Q Liu
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Abstract

Aim: To evaluate the effects of L-pyroglutamic acid (L-PGA, L-5-oxo-2-pyrrolidinecaroxylic acid) on sodium glutamate-induced neurotoxicity in rat cortical neurons.

Methods: In primary cortical cultures from 16-d-old fetal rat, neuronal viability and contents of nitrite in the bathing medium after transient exposure to sodium glutamate (Glu) were measured; with Fura 2-AM as an intracellular calcium indicator, AR-CM-MIC cation measurement system was used to examine cytosolic free calcium ([Ca2+]i).

Results: L-PGA 10-80 mumol.L-1, inhibited Glu (500 mumol.L-1)-induced neuronal loss in a concentration-dependent manner with IC50 value of (41 +/- 9) mumol.L-1 (95% confidence limits: 30.3-54.7 mumol.L-1). L-PGA also attenuated Glu-induced NO release. L-PGA 1, 3, 10, 30, and 100 mumol.L-1 depressed Glu-caused [Ca2+]i elevation by 20.5%, 34.4%, 47.7%, 70.6%, and 80.4%, respectively.

Conclusion: L-PGA protects cortical neurons against Glu-induced neurotoxity which may be related to inhibition of NO formation or suppression of the rise in [Ca2+]i.

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l -焦谷氨酸保护大鼠皮层神经元免受谷氨酸钠诱导的损伤。
目的:探讨l -焦谷氨酸(L-PGA, l -5-氧-2-吡咯烷甲酸)对谷氨酸钠诱导的大鼠皮质神经元神经毒性的影响。方法:测定16 d龄胎鼠皮层原代培养物短暂暴露于谷氨酸钠(Glu)后,沐浴液中神经元活力和亚硝酸盐含量;以Fura 2-AM为胞内钙离子指示剂,采用AR-CM-MIC阳离子测量系统检测胞内游离钙([Ca2+]i)。结果:L-PGA 10 ~ 80 μ mol。L-1抑制Glu (500 μ mol.L-1)诱导的神经元损失,IC50值为(41 +/- 9)μ mol。L-1(95%置信限:30.3-54.7 mmol .L-1)。L-PGA也能减弱葡萄糖诱导的NO释放。L-PGA 1,3,10,30和100 μ mol。L-1抑制的glu引起的[Ca2+]i升高分别为20.5%、34.4%、47.7%、70.6%和80.4%。结论:L-PGA可保护皮质神经元免受glu诱导的神经毒性,其机制可能与抑制NO形成或抑制[Ca2+]i升高有关。
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Supraspinal D2 receptor involved in antinociception induced by l-tetrahydropalmatine. CYP2D6 phenotype determines pharmacokinetic variability of propafenone enantiomers in 16 HAN Chinese subjects. Subtypes of central nicotinic receptors involved in learning and memory. Effects of tetrandrine on changes of NMDA receptor channel in cortical neurons of rat induced by anoxia. L-pyroglutamic acid protects rat cortical neurons against sodium glutamate-induced injury.
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