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, thereby inhibiting aggregations of Aβ42. In addition, an SH-SY5Y 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 contents 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.
ZHANG Jing
,
HUANG Jian'an
,
CAI Shuxian
,
YI Xiaoqin
,
LIU Jianjun
,
WANG Yingzi
,
TIAN Lili
,
LIU Zhonghua
. Theaflavins and EGCG Protect SH-SY5Y Cells from Oxidative Damage Induced by Amyloid-β 1-42 and Inhibit the Level of Aβ42 in vivo and in vitro[J]. Journal of Tea Science, 2016
, 36(6)
: 655
-662
.
DOI: 10.13305/j.cnki.jts.2016.06.013
[1] Schmaier A H.Alzheimer disease is in part a thrombohemorrhagic disorder[J]. Journal of Thrombosis and Haemostasis, 2016, 14(5): 991-994.
[2] Hardy J, Selkoe D J.The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics[J]. Science, 2002, 297(5580): 353-356.
[3] Fernandez-Echevarria C, Diaz M, Ferrer I, et al.Aβ promotes VDAC1 channel dephosphorylation in neuronal lipid rafts. Relevance to the mechanisms of neurotoxicity in Alzheimer’s disease[J]. Neuroscience, 2014, 278: 354-366.
[4] Vitek M P, Bhattacharya K, Glendening J M, et al.Advanced glycation end products contribute to amyloidosis in Alzheimer disease[J]. Proceedings of the National Academy of Sciences, 1994, 91(11): 4766-4770.
[5] da Silva Pinto M. Tea: A new perspective on health benefits[J]. Food Research International, 2013, 53(2): 558-567.
[6] Frei B, Higdon J V.Antioxidant activity of tea polyphenols in vivo: evidence from animal studies[J]. Journal of Nutrition, 2003, 133(10): 3275S-3284S.
[7] Balentine D A, Wiseman S A, Bouwens L C, et al.The chemistry of tea flavonoids[J]. Critical Reviews in Food Science & Nutrition, 1997, 37(8): 693-704.
[8] Bastianetto S, Yao Z X, Papadopoulos V, et al.Neuroprotective effects of green and black teas and their catechin gallate esters against β-amyloid-induced toxicity[J]. European Journal of Neuroscience, 2006, 23(1): 55-64.
[9] Grelle G, Otto A, Lorenz M, et al.Black tea theaflavins inhibit formation of toxic amyloid-β and α-synuclein fibrils[J]. Biochemistry, 2011, 50(49): 10624-10636.
[10] Bieschke J, Russ J, Friedirich R P, et al.EGCG remodels mature α-synuclein and amyloid-β fibrils and reduces cellular toxicity[J]. Proceedings of the National Academy of Sciences, 2010, 107(17): 7710-7715.
[11] Ehrnhoefer D E, Bieschke J, Boeddrich A, et al.EGCG redirects amyloidogenic polypeptides into unstructured, off-pathway oligomers[J]. Nature structural & molecular biology, 2008, 15(6): 558-566.
[12] 高雄, 陈忠正, 张媛媛, 等. 茶叶活性成分对阿尔茨海默症的神经保护作用研究进展[J]. 现代食品科技, 2015, 31(12): 416-425.
[13] 魏然, 徐平, 应乐, 等. 茶多酚对阿尔茨海默病的防治功能与机理研究进展[J]. 茶叶科学, 2016, 36(1): 1-10.
[14] Yang Z, Jie G, Dong F, et al.Radical-scavenging abilities and antioxidant properties of theaflavins and their gallate esters in H2O2-mediated oxidative damage system in the HPF-1 cells[J]. Toxicology in Vitro, 2008, 22(5): 1250-1256.
[15] Halder J and Bhaduri A N. Protective role of black tea against oxidative damage of human red blood cells[J]. Biochemical and Biophysical Research Communications, 1998, 244(3): 903-907.
[16] 刘晓慧, 揭国良, 林康, 等. EGCG和茶氨酸对细胞氧化损伤的协同保护和修复作用研究[J]. 茶叶科学, 2014, 34(3): 239-247.
[17] Leung L K, Su Y, Chen R, et al.Theaflavins in black tea and catechins in green tea are equally effective antioxidants[J]. The Journal of Nutrition, 2001, 131(9): 2248-2251.
[18] 李松, 刘夫锋, 余林玲, 等. 硫黄素T对淀粉样β-蛋白质40聚集成核动力学的双重影响[J]. 物理化学学报, 2016, 32(6): 1391-1395.
[19] 张静, 蔡淑娴, 黄建安, 等. 茶黄素对BSA/MDA羰-氨交联反应体系中的蛋白质羰基化及其聚集化抑制作用研究[J]. 茶叶科学, 2016, 36(4): 363-371.
[20] Lee S J, Lee K W.Protective effect of (-)-epigallocatechin gallate against advanced glycation endproducts-induced injury in neuronal cells[J]. Biological & Pharmaceutical Bulletin, 2007, 30(8): 1369-1373.
[21] Mustata G T, Rosca M, Biemel K M, et al.Paradoxical effects of green tea (Camellia sinensis) and antioxidant vitamins in diabetic rats: improved retinopathy and renal mitochondrial defects but deterioration of collagen matrix glycoxidation and cross-linking[J]. Diabetes, 2005, 54(2): 517-526.
[22] Shuvaev V V, Laffont I, Serot JM, et al.Increased protein glycation in cerebrospinal fluid of Alzheimer’s disease[J]. Neurobiology of aging, 2001, 22(3): 397-402.
[23] Loske C, Gerdemann A, Schepl W, et al.Transition metal-mediated glycoxidation accelerates cross-linking of β-amyloid peptide[J]. European Journal of Biochemistry, 2000, 267(13): 4171-4178.
[24] 李大祥, 鲜殊, 杨卫, 等. 茶叶的神经保护作用研究进展[J]. 茶叶科学, 2011, 31(2): 79-86.
[25] 刘春芳. 表没食子儿茶素没食子酸酯抗氧化及神经元保护作用的研究进展[J]. 蚌埠医学院学报, 2011, 36(10): 1163-1164.
浙公网安备 33019902000101号 
