丁基苯酞抗大鼠大脑皮质神经元氧糖剥夺/复氧损伤及其机制

本研究探讨丁基苯酞抗大鼠大脑皮质神经元氧糖剥夺/复氧损伤及其机制。原代培养大鼠大脑皮质神经元，建立氧糖剥夺/复氧模型(OGD/R)，采用MTT法、酶学检查、免疫组化、RT-PCR等观察丁基苯酞(各浓度组)的保护作用及其机制。在氧糖剥夺4 h/复氧8 h时丁基苯酞各浓度组可增加神经元的细胞活力和减少神经元LDH(乳酸脱氢酶)的释放，可显著降低神经元表达iNOS mRNA(诱生型一氧化氮合酶)和NF-κB(核因子κB) p65蛋白(增加)。不同剂量丁基苯酞(100、 10、 1和0.1 μmol·L^-1)在增加细胞活力、减少LDH释放及降低神经元表达iNOS mRNA等方面，高浓度的作用强于低浓度，且丁基苯酞100 μmol·L^-1组与吡咯烷二硫代氨基甲酸酯(pyrrolidine dithiocarbamate，PDTC) 100 μmol·L^-1组差异显著。在OGD 4 h/R 8 h时丁基苯酞可能抑制iNOSmRNA的表达及NF-κB的活化，从而有效保护氧糖剥夺/复氧中损伤的大脑皮质神经元。

Mechanism of action of butylphalide against the injury following oxygen glucose deprivation/reoxygenation in rat cortical neurons

To explore the mechanism of action of butylphalide (NBP) against the injury following oxygen glucose deprivation/reoxygenation (OGD/R) in rat cortical neurons, neurons of Wistar newborn rats were prepared by filtering through a mesh, centrifugation and trypsogen digestion. A simple, stable and reliable in vitro model of OGD/R of neurons was established. We studied the activation, the nuclear translocation of NF-kappaB p65 and the mRNA expression of iNOS affected by NBP in each group neuron by RT-PCR. NBP is proved to be able to add cellular vigor and decrease LDH release. The mRNA expression of iNOS in neurons after OGD 4 h/R 8 h decreased when treated with NBP. There is statistical difference between each concentration of NBP that it adds cellular vigor, decreases LDH release and expression of iNOS in neurons after OGD 4 h/R 8 h. There is also statistical difference between NBP (100 micromol x L(-1)) and PDTC (100 micromol x L(-1)). It is proved that NBP can protect neurons, block upregulation of iNOS mRNA, and restrain activation of NF-kappaB in neurons.