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

WANG Qiu-yue; GAO Xiang; WANG Xiao-ling; ZHANG Ling-yan

doi:10.13422/j.cnki.syfjx.2014240164

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

更新时间：2024-01-04

- Neuroprotective Effects and Mechanism of Taxifolin Against Neural Damage Induced by A
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 20, Issue 24, Pages: 164-167(2014)
- 作者机构：
- 作者简介：
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- DOI：10.13422/j.cnki.syfjx.2014240164
  CLC： R285.5
- Published：2014
- 稿件说明：
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WANG Qiu-yue, GAO Xiang, WANG Xiao-ling, et al. Neuroprotective Effects and Mechanism of Taxifolin Against Neural Damage Induced by A[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(24): 164-167.
DOI：

WANG Qiu-yue, GAO Xiang, WANG Xiao-ling, et al. Neuroprotective Effects and Mechanism of Taxifolin Against Neural Damage Induced by A[J]. Chinese journal of experimental traditional medical formulae, 2014, 20(24): 164-167. DOI： 10.13422/j.cnki.syfjx.2014240164.

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(5 μmol·L-1)、不同浓度花旗松素(20~100 μmol·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80 μmol·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40 μmol·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

40 μmol·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.

Abstract

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 caspase-3 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.

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