YUAN Fang, ZHOU Yong, SHENG Lei, et al. Effect of Polysaccharide from on Expression of APP in Alzheimer's Disease Cell Model[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(18): 107-110.
DOI:
YUAN Fang, ZHOU Yong, SHENG Lei, et al. Effect of Polysaccharide from on Expression of APP in Alzheimer's Disease Cell Model[J]. Chinese journal of experimental traditional medical formulae, 2015, 21(18): 107-110. DOI: 10.13422/j.cnki.syfjx.2015180107.
Effect of Polysaccharide from on Expression of APP in Alzheimer's Disease Cell Model
VTP)对β-淀粉样蛋白25-35 (Aβ25-35)诱导PC12细胞β-淀粉样前体蛋白(beta-amyloid precursor protein
APP)基因表达的影响
探讨VTP在阿尔茨海默病(Alzheimer's disease
AD)发病机制中的作用。方法: 体外培养PC12细胞
分为对照组
AD模型组(20 μmol·L-1Aβ25-35作用24 h)
VTP低、中、高剂量组质量浓度分别为20
40
80 mg·L-1。VTP作用24 h后
检测细胞活性、超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量和细胞超微结构
采用实时荧光定量PCR(real-time PCR)检测APP mRNA表达。结果: 与正常组比较
模型组细胞活性及SOD活力降低(P<0.01)
MDA含量及APP mRNA表达增高(P<0.01)
细胞超微结构明显异常;与模型组比较
给药组细胞活性及SOD活力增强(P<0.05)
MDA含量及APP mRNA表达下降(P<0.01)
减轻神经细胞损伤。结论: VTP对Aβ25-35诱导的氧化损伤有保护作用
通过抗氧化和调节APP mRNA表达
抑制Aβ形成
保护神经细胞
起到防治AD的作用。
Abstract
Objective: To investigate protective effect of polysaccharide from Vitis viniferal (VTP) on expression of beta-amyloid precursor protein (APP) in PC12 cells induced by β-amyloid protein25-35(Aβ25-35)
in order to discuss the mechanism of VTP in pathogenesis of Alzheimer's disease (AD). Method: Alzheimer's disease (AD) cell model was established by inducing PC12 cells with 20 μmol· L-1 Aβ25-35 for 24 h and intervened with different concentrations of VTP (20
40
80 mg· L-1). Cell viability was detected by CCK-8.The activities of dismutase superoxide(SOD) and malondialdehyde(MDA) were measured. The expression of APP mRNA was quantified by real-time PCR. Result: Compared with the normal group
the model group showed decreases in cell viability and SOD activity (P<0.01) and increases in MDA content and APP mRNA expression (P<0.01). Compared with the model group
cell viability and SOD activity were increased (P<0.05)
MDA content and APP mRNA expression were decreased in VTP groups (P<0.05)
indicating the relief in neuronal injury. Conclusion: VTP has a protective effect in the oxidative injury induced by Aβ25-35 and plays a role in preventing and treating AD by resisting oxidation
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Hei Xiaoyaosan Inhibits Ferroptosis by Regulating SIRT1/p53/SLC7A11 Signaling Pathway to Ameliorate Cognitive Dysfunction in Rat Model of Alzheimer's Disease
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