西红花酸对Aβ_(25-35)诱导海马神经元损伤的神经保护作用

Neuroprotection of Crocetin on Amyloid β_(25-35)-induced Neurotoxicity in Cultured Hippocampal Neurons

目的探讨西红花酸对Aβ_25-35诱导的SD大鼠海马神经元损伤的神经保护作用。方法常规培养SD大鼠海马神经元,分为对照组、0.1μM西红花酸组、10μmol/L Aβ_25-35组、0.01μM西红花酸+10μmol/L Aβ_25-35组、0.1μM西红花酸+10μmol/L Aβ_25-35组、1μM西红花酸+10μmol/L Aβ_25-35组;MTT检测细胞活力变化情况;荧光探针DCFH-DA检测细胞内ROS水平变化情况。结果 10μmol/L Aβ_25-35显著降低细胞的活性和升高海马神经元ROS水平(P<0.01);不同浓度西红花酸(0.01、0.1和1μM)预处理后,细胞活性分别比Aβ_25-35组提高了39.2%、56.1%和76.4%,差异有显著性意义(P<0.05),培养10天和25天海马神经元的ROS水平与Aβ_25-35组比较均显著降低(P<0.01)。结论西红花酸对Aβ_25-35诱导海马神经元的损伤具有保护作用,能显著降低Aβ_25-35引起的海马神经元ROS水平的升高。

Objective To explore the neuroprotective effects of crocetin on amyloid β25-35-induced neurotoxicity in cultured hippocampal neurons. Methods Hippocampal neurons derived from 4 weeks old SD rats were cultured and divided into six groups： the control group, 0.1uM crocetin group, 10 umol/L Aβ25-35 group, 0.01uM crocetin ＋ 10 umol/L Aβ25-35 group, 0.1uM crocetin ＋ 10umol/L Aβ25-35 group, 1uM crocetin ＋ 10umol/L Aβ25-35 group. Cell viability and ROS levels in hippocampal neurons were respectively detected by MTT assay and fluorescent probe DCFH-DA. Results After treatment with 10 umol/L Aβ25-35, cell viability significantly decreased and ROS levels significantly increased （P 〈0.01）. However, cell viability of the group pre-cultured with crocetin significantly increased （P 〈0.05 compared with Aβ25-35 group）, and ROS levels significantly decreased （P 〈0.01 compared with Aβ25-35 group）. Conclusion Crocetin can attenuate Aβ25-35-induced neuronal damage, increase cell viability and decrease ROS levels in cultured hippocampal neurons of SD rats.