紅景天苷具有對抗缺氧、缺血、糖尿病腦病、β 淀粉樣肽和老齡引起的動物癡呆作用,綜述其抗癡呆作用及作用機(jī)制研究進(jìn)展。其抗癡呆作用機(jī)制主要包括3 個方面;(1)通過抑制缺氧誘生因子-1α 和淀粉樣前體蛋白β 位裂解酶1 的表達(dá)以及β-分泌酶活性,阻滯β 淀粉樣肽生成;(2)通過抗氧化作用而阻滯β 淀粉樣肽、晚期糖基化終產(chǎn)物、缺血、缺氧、H2O2等引起的氧化應(yīng)激反應(yīng)和細(xì)胞內(nèi)鈣超載發(fā)生,保護(hù)神經(jīng)干細(xì)胞和神經(jīng)細(xì)胞免遭傷害;(3)通過阻滯Notch 信號轉(zhuǎn)導(dǎo)通路,促進(jìn)BMP 信號轉(zhuǎn)導(dǎo)通路和磷脂酰肌醇3-激酶依賴的Ca²⁺信號轉(zhuǎn)導(dǎo),誘導(dǎo)間充質(zhì)干細(xì)胞和神經(jīng)干細(xì)胞定向分化成神經(jīng)元,從而促進(jìn)神經(jīng)發(fā)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.