红景天苷的神经保护作用及作用机制研究进展

Research progress on neuroprotective effect and mechanism of salidroside

动物实验结果显示红景天苷对多种原因引起的神经细胞和脑组织损伤均有保护作用,有望用于周围神经损伤以及脑缺血性和神经变性疾病(如脑梗死、老年痴呆、帕金森病、癫痫、抑郁、抽动秽语综合征、肌萎缩性侧索硬化症和糖尿病脑病等)的防治。其神经保护作用机制主要包括3个方面:(1)通过抗氧化作用,抑制NOX2/ROS/MAPKs和REDD1/m TOR/p70S6K信号通路,激活AMPK/SIRT1、Rho A-MAPK和PI3K/Akt信号通路,对抗各种损伤因子引起的氧化应激,抑制炎性细胞因子表达,防止细胞内Ca^(2+)超载和半胱天冬酶-3活化,保护神经细胞和干细胞免遭凋亡性损伤;(2)抑制淀粉样前体蛋白β位裂解酶-1的表达和β-分泌酶活性,阻滞内源性伤害因子β-淀粉样肽生成;(3)通过阻滞Notch信号通路,促进BMP信号通路,上调多种神经营养因子表达,诱导间充质干细胞和神经干细胞定向分化成神经元,提高许旺细胞增殖和功能,从而加速神经修复、再生和功能恢复。

Some animal model experiments have found that salidroside has protective effect for injuries in various neurons and brain tissue induced by various causes, so it is expected to be used in the prevention and treatment of peripheral nerve injury, and cerebral ischemic and neurodegenerative diseases, such as cerebral infarction, Alzheimer＇s disease, Parkinson＇s disease, epilepsy, depression, Tourette syndrome, amyotrophic lateral sclerosis, and diabetic encephalopathy. Its mechanisms of neuroprotection are multiple： （1） Salidroside protects neurons and stern cells from apoptotic injury by antioxidation, blocking NOX2/ROS/MAPKs and REDD 1/mTOR/p70S6K signaling pathways, and promoting AMPK/SIRT1, RhoA-MAPK and PI3K/Akt signaling pathways against various injurious factors-induced oxidative stress, inhibiting expression of inflammatory cytokines, preventing intracellular Ca^2＋ overload and caspase-3 activation; （2） Salidroside obstructs endogenous amyloid-β production by inhibition of expression of β-site amyloid precursor protein cleaving enzyme 1 and β-secretase activity. （3） Salidroside accelerates repair, regeneration and functional recovery of nerve by block Notch signaling pathway, and promoting BMP signaling pathway, super-regulating expression of neurotrophic factors, inducing neural stem ceils and mesenchymal stem cells to differentiate into neural cells, and improving proliferation and fimction of Schwann cells.