摘要
红景天苷具有对抗缺氧、缺血、糖尿病脑病、β淀粉样肽和老龄引起的动物痴呆作用,综述其抗痴呆作用及作用机制研究进展。其抗痴呆作用机制主要包括3 个方面:(1)通过抑制缺氧诱生因子-1α和淀粉样前体蛋白β位裂解酶1 的表达以及β-分泌酶活性,阻滞β淀粉样肽生成;(2)通过抗氧化作用而阻滞β淀粉样肽、晚期糖基化终产物、缺血、缺氧、H2O2等引起的氧化应激反应和细胞内钙超载发生,保护神经干细胞和神经细胞免遭伤害;(3)通过阻滞Notch 信号转导通路,促进BMP 信号转导通路和磷脂酰肌醇3-激酶依赖的Ca2+信号转导,诱导间充质干细胞和神经干细胞定向分化成神经元,从而促进神经发生。
Salidroside has the effects against hypoxia-, ischemia-, diabetic encephalopathy-, amyloid-β-, and aging-induced dementia in animals. The mechanisms of its anti-dementia were as follows. (1) Salidroside obstructs amyloid-β production by inhibition of expression of β-site amyloid precursor protein cleaving enzyme 1 and hypoxia-inducible factor 1, and β-secretase activity.(2) Salidroside protects neural stem cells and neural cells (inclusion of hippocampal neurons) from injury by its antioxidation to obstruct amyloid-β-, advanced glycation end products-, ischemia-, hypoxia-, H2O2-induced oxidative stress and intracellular calcium overload occurrence. (3) Salidroside induces neural stem cells and bone marrow mesenchymal stem cells to differentiate into neural cells by blocking Notch signaling pathway, and promoting BMP signaling pathway and PI3K dependent Ca2+ signaling pathway, and enhances neurogenesis thereby.
出处
《药物评价研究》
CAS
2015年第6期675-681,共7页
Drug Evaluation Research
