人参茎叶人参皂苷对东莨菪碱所致记忆损伤的保护作用及其分子机制研究。

Ying Wang, Junjun Zhang, Jingang Hou, Xin Li, Wei Liu, Jing-tian Zhang, Si-Wen Zheng, Feng-Yan Su, Wei Li
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引用次数: 4

摘要

尽管越来越多的证据表明,人参茎叶中的人参皂苷对中枢神经系统具有保护作用,但在东莨菪碱诱导的记忆损伤模型中,这一点仍然很少报道。因此,需要进一步探讨行动机制。本研究旨在探讨GSLS对东莨菪碱(SCOP)诱导的记忆损伤的影响及其潜在机制。雄性ICR小鼠用SCOP(3 mg/kg)治疗7天,用或不用GSLS(75和150 mg/kg)治疗14天。GSLS治疗后,SCOP诱导的记忆损伤显著改善,表现为胆碱能功能(AChE和ChAT)、脑组织海马形态(H&E染色)和氧化应激(MDA、GSH和NO)的改善。同时,免疫组织化学分析表明,GSLS增加了脑源性神经营养因子(BDNF)和酪氨酸激酶受体B(TrkB)的表达。进一步的机制研究表明,GSLS通过调节PI3K/AKT通路抑制Tau过度磷酸化和细胞凋亡,并通过调节NF-[公式:见正文]B通路抑制神经炎症,从而发挥改善认知障碍的作用。这项工作表明,GSLS可能通过抑制氧化应激、抑制神经炎症和细胞凋亡来预防SCOP诱导的记忆缺陷。
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Protective Effect of Ginsenosides from Stems and Leaves of Panax ginseng against Scopolamine-Induced Memory Damage via Multiple Molecular Mechanisms.
Although growing evidence has shown that ginsenosides from stems and leaves of Panax ginseng (GSLS) exercise a protective impact on the central nervous system, in the model of memory damage induced by scopolamine, it is still rarely reported. Thus, the mechanism of action needs to be further explored. This study was to investigate the effect of GSLS on scopolamine (SCOP)-induced memory damage and the underlying mechanism. Male ICR mice were treated with SCOP (3 mg/kg) for 7 days, with or without GSLS (75 and 150 mg/kg) treatment for 14 days. After GSLS treatment, the memory damage induced by SCOP was significantly ameliorated as shown by the improvement of cholinergic function (AChE and ChAT), brain tissue hippocampus morphology (H&E staining), and oxidative stress (MDA, GSH, and NO). Meanwhile, immunohistochemical assay suggested that GSLS increased the expression of brain-derived neurotrophic factor (BDNF) and Tyrosine Kinase receptor B (TrkB). Further mechanism research indicated that GSLS inhibited the Tau hyperphosphorylation and cell apoptosis by regulating the PI3K/AKT pathway and inhibited neuroinflammation by regulating the NF-[Formula: see text]B pathway, thereby exerting a cognitive impairment improvement effect. This work suggested that GSLS could protect against SCOP-induced memory defects possibly through inhibiting oxidative stress, inhibiting neuroinflammation and cell apoptosis.
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