左旋丁基苯酞在体外模拟脑缺血再灌注诱导的神经元损伤中的保护作用

Protective effect of L-butylphthalide on nerve cell injury induced by mimic ischemia reperfusion in vitro

目的探讨左旋丁基苯酞(L-NBP)在体外模拟脑缺血再灌注诱导神经元损伤中的保护作用及机制。方法缺血再灌注模型建立后,用不同浓度的L-NBP(1、10、100μmol/L)干预大鼠皮质神经元,倒置显微镜下观察细胞形态,MTT法测定细胞活性率,免疫印迹法检测核转录因子-κB(NF-κB)、bcl-2、bax、Caspasce-3凋亡调节蛋白的变化。结果L-NBP可明显改善神经元生长形态、活性率,抑制NF-κB、Caspasce-3表达,下调bax/bcl-2比值,且随浓度增加而作用更强(P<0.05、<0.01)。结论L-NBP对在体外模拟脑缺血再灌注诱导的神经元损伤中的保护作用可能与其抑制NF-κB活化及Caspasce-3表达,下调bax/bcl-2比值有关。

Objective To investigate the protective effect and mechanism of L-butylphthalide on nerve cell induced by mimic ischemia reperfusion in vitro. Methods After ischemia reperfusion model was established, rat cerebral cortical neu- rons were treated with L-butylphthalide in different concentration（ 1,10,100μmol/L）. The neurons shape was observed with inverted microscope , MTr methods was used to detect cytoactive. The apoptosis regulation protein NF-kB, bcl-2, bax, Caspasce-3 were detected by western blot. Results L-butylphthalide could improve the growth status of the neurons, liveness, and suppress the expression of NF-KB, Caspasce-3 , down regulate bcl-2/bax value,and the effects became more and more strong with the density of L-NBP increasing（ P 〈 0.05,0.01 ）. Conclusions L-butylphthalide can protect neu-rons from injury during ischemia-reperfusion in vitro by suppressing activation of NF-KB, Caspasce-3 expressions and down regulating bcl-2/bax value.