第10号染色体缺失的磷酸酶和张力蛋白在谷氨酸诱导海马神经元损伤中的作用研究

目的：探讨第10号染色体缺失的磷酸酶和张力蛋（PTEN）在谷氨酸（Glu）诱导海马神经元损伤的作用及机制。方法：选用新生Wistar大鼠原代培养海马神经元，建立Glu细胞毒性损伤模型，采用RT—PCR，PI染色检测神经元损伤后PTEN表达的变化，以及PTEN抑制剂对神经元损伤的保护作用，同时通过激光扫描共聚焦显微镜检测细胞内Ca^2＋浓度的变化。结果：Glu诱导神经元损伤后，PTEN的表达增加，通过抑制PTEN活性可减少神经元的死亡，并在一定程度上抑制Glu诱导的神经元Ca^2＋内流。结论：磷酸酶PTEN参与了神经元的损伤过程，利用bpv抑制PTEN的活性可对Glu诱导的神经元损伤具有保护作用，其中抑制Glu引起的神经元Ca^2＋内流可能是其保护机制之一。

Effects of the Phosphatase and Tensin Homologue Deleted on Chromosome 10 on Hippocampus Neurons Injury Caused by Glutamate

Aim：To study the effects of the phosphatase and tensin homologue deleted on chromosome 10 （PTEN） on hippocampus neuron injury caused by glutamate and their mechanism. Methods： Glutamate cytotoxicity model of primary culture neurons from neonatal Wistar rat hippocampus was used to evaluate the expression of PTEN and protective effects of PTEN inhibitor on neuron injury through RT-PCR and PI dye. Intracellular Ca^2＋ current was determined with laser scanning confocal microscopy. Results： The expression of PTEN increased after neuron injury caused by Glu. Blockage of PTEN can decrease the death of neuron and inhibit Ca^2＋ influx caused by Glu. Conclusion： PTEN attended the process of neuron injury and bpv can produce protective effect on injured neurons caused by Glu through inhitibiting the activity of PTEN, among which decreasing Ca^2＋ influx induced by Glu may be one kinds of mechanism of bpv against Glu exciting toxicity.