【摘要】 通过模拟生理条件体外实验,将β-淀粉样蛋白1-42（Aβ42）与EGCG和4种茶黄素单体分别按照1︰1和1︰5比例进行孵育,采用硫黄素T荧光检测β-折叠结构的生成量,结果表明,EGCG与茶黄素均能明显降低β-折叠结构生成,从而抑制Aβ42聚集;此外,通过建立20μmol·L^-1 Aβ42诱导人神经母细胞瘤SH-SY5Y细胞损伤模型,将不同浓度的EGCG或茶黄素(10、50、100μmol·L^-1)处理后,MTT法检测细胞存活率,同时,检测细胞内活性氧（ROS）、谷胱甘肽过氧化物酶（GSH-Px）及丙二醛（MDA）等抗氧化指标,结果表明,EGCG与茶黄素可抑制因Aβ42诱导SH-SY5Y细胞活力下降及氧化损伤。体内实验中,通过10mg·kg^-1·d^-1的EGCG或茶黄素处理快速老化模型小鼠（SAMP8）,10周后检测小鼠血清Aβ42及晚期糖基化终末产物（AGEs）含量,结果表明,EGCG和茶黄素可显著降低SAMP8小鼠血清中Aβ42及AGEs含量。本研究表明了茶黄素和EGCG可抑制Aβ42聚集纤维化及Aβ42导致的神经氧化损伤,从而对阿尔茨海默病具有一定保护作用。更多还原

【Abstract】 In this study, amyloid β-protein Aβ42 was incubated with EGCG, TF, TF-3-G, TF-3’-G, TF-DG at the ratio of 1:1 and 1:5 under simulated physiological condition. The contents of β-sheets after incubation were tested by thioflavin T fluorometric assay. It was found that EGCG and theaflavins could suppress the formation of β-sheet structure, therebyinhibiting aggregations of Aβ42. In addition, an SH-SY5 Y cell damage model was established and MTT assay was used to examine cell viabilities when 20 μmol·L-1 Aβ42 was incubated with different concentrations of EGCG and theaflavins(10, 50, 100 μmol·L-1). Intracellular reactive oxygen species(ROS) levels, antioxidant enzyme activities(GSH-Px) and MDA levels were also measured. The results showed EGCG and theaflavins treatments could alleviate the Aβ42 induced oxidative damage to neural cells by reducing ROS and increasing the activity of GSH-Px. To study the in vivo protective effects of EGCG and theaflavins, SAMP8 mice were treated with 10 mg·kg-1·d-1 EGCG or theaflavins respectively by gavage for 10 weeks, and the contents of Aβ42 and AGEs in mouse serum were determined. The results showed that EGCG and theaflavins significantly decreased the content s of Aβ42 and AGEs in SAMP8 serum. In summary, EGCG and theaflavins could inhibit the aggregations of Aβ42 and reduce oxidative injury induced by Aβ42 in neural cells, thereby exerting protective effects on AD.更多还原