Department of Pathophysiology, Institute of Basic Medicine, Hebei Medical University, 361 Zhongshan East Road, Shijiazhuang 050017, People's Republic of China.
Neurochem Res. 2011 Oct;36(10):1724-31. doi: 10.1007/s11064-011-0487-1. Epub 2011 May 10.
Several mechanisms are involved in the neuroprotection of propofol against ischemia, but influences of propofol on the binding properties of glutamate receptors and the uptake of glutamate in brain ischemia are not known. The present study was undertaken to investigate these issues in rat global brain ischemic model using methods of neuropathological evaluation, radioligand binding assay with and uptake test for L-(3)H-glutamate. It was shown that propofol used in anesthetic doses protected pyramidal neurons in the hippocampal CA1 subfield against delayed neuronal death normally induced by global brain ischemia. Simultaneously, the propofol decreased the value of maximal number of binding sites (Bmax), increased the value of equilibrium dissociation constant (Kd), and increased the glutamate uptake in the CA1 subfield. These findings indicate that it is, at least partly, via modulating the binding properties of glutamate receptors and the uptake of glutamate that propofol protects neurons against ischemic injury.
几种机制参与了异丙酚对缺血的神经保护作用，但异丙酚对谷氨酸受体结合特性和脑缺血中谷氨酸摄取的影响尚不清楚。本研究采用神经病理评估、放射性配体结合测定和 L-（3）H-谷氨酸摄取测定方法，在大鼠全脑缺血模型中探讨了这些问题。结果表明，麻醉剂量的异丙酚可保护海马 CA1 区锥体神经元免受全脑缺血正常诱导的迟发性神经元死亡。同时，异丙酚降低了最大结合位点数量（Bmax）的值，增加了平衡解离常数（Kd）的值，并增加了 CA1 区的谷氨酸摄取。这些发现表明，异丙酚通过调节谷氨酸受体的结合特性和谷氨酸的摄取来保护神经元免受缺血性损伤，至少部分是通过这种方式。
