Alpha-tocopherol quinone inhibits beta-amyloid aggregation and cytotoxicity, disaggregates preformed fibrils and decreases the production of reactive oxygen species, NO and inflammatory cytokines

作者：Yang, Shi-gao; Wang, Wei-yun; Ling, Tie-jun; Feng, Ying; Du, Xue-ting; Zhang, Xi; Sun, Xiao-xia; Zhao, Min; Xue, Di; Yang, Yang; Liu, Rui-tian^*

来源：Neurochemistry International, 2010, 57(8): 914-922.

DOI：10.1016/j.neuint.2010.09.011

• Alzheimer's disease
• Amyloid beta protein
• RRR alpha tocopherol quinine
• Aggregation
• Cytotoxicity
• Inflammatory cytokines

Alzheimer s disease (AD) is a complex multifactorial neurodegenerative disease The aggregation of beta-amyloid (A beta) into extracellular fibrillar deposition is a pathological hallmark of AD The A beta aggregate-induced neurotoxicity inflammatory reactions and oxidative stress are linked strongly to the etiology of AD The currently available hitting-one-target drugs are insufficient for the treatment of AD Therefore finding multipotent agents able to modulate multiple targets simultaneously is attracting more attention Previous studies indicated that vitamin E or its constituent such as alpha-tocopherol (alpha-T) was able to attenuate the effects of several pathogenetic factors in AD However ineffective or detrimental results were obtained from a number of clinical trials of vitamin E Here we showed that naturally synthesized RRR-alpha-tocopherol quinone (alpha-TQ) a main derivative of alpha-T could inhibit A beta 42 fibril formation dose-dependently Further investigations indicated that alpha-TQ could attenuate A beta 42-induced neurotoxicity toward SH-SY5Y neuroblastoma cells disaggregate preformed fibrils and interfere with natural intracellular A beta oligomer formation Moreover alpha-TQ could decrease the formation of reactive oxygen species (ROS) and NO and modulate the production of cytokines by decreasing TNF-alpha and IL-1 beta and increasing

• 出版日期2010-12
• 单位安徽农业大学; 清华大学