花旗松素对β-淀粉样肽损伤神经元的保护作用及机制  

Neuroprotective Effects and Mechanism of Taxifolin Against Neural Damage Induced by Aβ

作　　者：王秋月[1] 高翔[1] 王晓玲[1] 张玲艳[1] 

机构地区：[1]天津医科大学第二医院,天津300211

出　　处：《中国实验方剂学杂志》2014年第24期164-167,共4页Chinese Journal of Experimental Traditional Medical Formulae

摘　　要：目的：研究花旗松素对β-淀粉样肽（β-amyloid peptide,Aβ）损伤神经元的保护作用及其机制。方法：从新生乳鼠大脑皮层中分离纯化神经元,与Aβ（5μmol·L^-1）、不同浓度花旗松素（20~100μmol·L^-1）共同孵育24 h,CCK8法检测细胞存活率,Hoechst 33258染色和Annexin V-FITC/PI检测细胞凋亡,分光光度法检测半胱天冬酶-3（caspase-3）活性的变化。结果：在细胞活力实验中,与正常组相比,模型组细胞活力显著下降（49.2±1.3）%,不同浓度的花旗松素可以提高神经元活力,其中80μmol·L^-1花旗松素给药组细胞活力增至（68.7±3.2）%,与模型组相比有极显著差异;细胞凋亡结果显示,与正常组相比较,模型组细胞凋亡率为（50.8±1.5）%（P〈0.01）,不同浓度的花旗松素给药组可以降低细胞凋亡率,其中40μmol·L^-1花旗松素凋亡率为（41.5±2.7）%,与模型组比较呈显著性差异（P〈0.05）;凋亡酶caspase-3的活性与正常组（0.12±0.02）U·μg^-1比较,模型组的caspase-3的活性升高（2.37±0.16）U·μg^-1,P〈0.01）,与模型组相比,40μmol·L^-1花旗松素组caspase-3显著降低（1.77±0.07）U·μg^-1,P〈0.01）。花旗松素能明显提高Aβ损伤神经元的细胞活力,抑制神经元的凋亡,降低凋亡酶caspase-3的活性。结论：花旗松素对Aβ损伤神经元具有保护作用,其机制可能与抑制caspase-3活性从而实现抗凋亡作用有关。Objective：To investigate the neuroprotective effects and mechanism of taxifolin against Aβ induced neural damage.Method：Primary neurons were isolated and purified from cerebral cortex of suckling mouse.The neurons were co-cultured with Aβ and taxifolin for 24 h.CCK8 method was used to test cell viability.The apoptosis was examined by Hoechst 33258 nuclear staining,Annexin V-FITC/PI double staining and caspase3 activity.Result：In cell viability,compared with the normal group,cell viability of model group decreased significantly （49.2 ± 1.3） %,different concentrations of taxifolin could improve the neuronal activity,the cell viability of 80 μmol ·L^-1 taxifolin increased to （68.7 ± 3.2）%,compared with the model group.Compared with the normal group,the apoptosis rate of model group was （50.8 ± 1.5）% （P 〈 0.01）,different concentrations of taxifolin could reduce the cell apoptosis rate,40 μmol ·L^-1 taxifolin apoptosis rate was （41.5 ± 2.7）%,compared with the model group （P 〈 0.05）.Compared with the normal group,in model group,caspase-3 activity was （2.37 ±0.16） U ·μg^-1 （P 〈 0.01）,compared with the model group,40 μmol ·L^-1 taxifolin group decreased the caspase-3 activity （1.77 ± 0.07） U · μg^-1 （P 〈 0.01）.CCK8 assay displayed that taxifolin obviously increased cell viability.Hoechst 33258 nuclear staining and Annexin V-FITC/PI double staining showed that taxifolin could significantly decrease apoptotic rate compared with the Aβ treated group.Taxifolin also inhibited caspase-3 activity of neurons induced by Aβ.Conclusion：Taxifolin possesses the neuroprotective effects on Aβ damaged neurons,which may be associated with inhibition of caspase-3 activity in neurons to against apoptosis.

关 键 词：花旗松素 神经元 Β-淀粉样肽 凋亡 

分 类 号：R285.5[医药卫生—中药学]