芪智消渴颗粒对MPTP诱导斑马鱼神经损伤的保护作用

The protective effect of QZXK in nerve injury using zebrafish model induced by MPTP

目的 利用斑马鱼和细胞模型探讨芪智消渴颗粒(QZXK)对神经损伤的保护作用。方法 选择受精后72h的野生型斑马鱼AB品系幼鱼,建立1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)斑马鱼神经损伤模型,用QZXK 5、10、25、50 mg·L^(-1)处理72h后,记录分析斑马鱼的运动轨迹和运动距离;利用MPTP处理PC12细胞,给予不同剂量的QZXK,MTT法测定神经瘤细胞的细胞活力,并测定线粒体膜电位和caspase-3蛋白的活性。结果 实验表明MPTP造模组,斑马鱼运动行为受到抑制,QZXK能明显逆转MPTP造成的游泳行为异常,提高斑马鱼的运动距离;细胞实验结果显示,QZXK能抑制MPTP引起的神经瘤细胞凋亡,促进细胞增殖,提高线粒体膜电位和降低caspase-3的表达。结论 QZXK对MPTP诱导的神经损伤具有保护作用,其作用机制可能与抑制神经细胞的凋亡有关,本实验为QZXK改善认知功能提供了一定的理论和实验基础。

Aim To investigate the protective effect of Qi ZhiX iaoke granules（QZXK） on nerve injury using zebrafish and nerve cell injury models. Methods The nerve injury model was established using wild zebrafish AB line,72 hours after fertilization treated with 1-methyl-4-phenyl-1,2,3,6-four pyridine（MPTP）.Then QZXK of different doses were administered for three days,and the trajectory of the zebrafish behavior was recorded and analyzed. Neuroblastoma PC12 cells were incubated with different concentrations of QZXK and MPTP,and the cell viability of PC12 cells was detected by MTT. The mitochondrial membrane potentialand expression of apoptosis related protein Caspase3 were measured by kits. Results Compared with control group,MPTP reduced the movement distance of zebrafish,and with the increase of concentration,QZXK promoted the movement distance and reversed the swimming behavior abnormality of zebrafish. Compared with control group,QZXK could inhibit the apoptosis induced by MPTP and promote the cell viability of PC12 cells with MPTP. QZXK improved the membranepotential and decreased the expression of Caspase3.Conclusions QZXK exerts neuroprotective effect in the process of nerve injury induced by MPTP. The mechanism may be related with inhibiting apoptosis of neural cells. These experiment provides experimental and theoretical foundation for QZXK promoting cognitive function.