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Cognitive-enhancing and ameliorative effects of acanthoside B in a scopolamine-induced amnesic mouse model through regulation of oxidative/inflammatory/cholinergic systems and activation of the TrkB/CREB/BDNF pathway
Food and Chemical Toxicology ( IF 3.9 ) Pub Date : 2019-05-08 , DOI: 10.1016/j.fct.2019.04.062
Govindarajan Karthivashan , Mee-Hyang Kweon , Shin-Young Park , Joon-Soo Kim , Deuk-Hoi Kim , Palanivel Ganesan , Dong-Kug Choi

Recently, our research team reported the anti-amnesic potential of desalted-hydroethanolic extracts of Salicornia europaea L. (SE-EE). In this study, we performed bioactivity-guided isolation and identification of Acanthoside B (Aca.B), from SE-EE, as the potential bioactive candidate and examined anti-amnesic activity with its potential mechanism of action using an in vivo model. S7-L3-3 purified from SE-EE showed enhanced in vitro acetylcholinesterase (AChE) inhibitory activity. The isolated S7-L3-3 was identified and characterized as Aca.B using varied spectral analyses, i.e., Nuclear magnetic resonance (NMR), Ultraviolet–visible (UV–Vis), and Electrospray ionization-mass spectrometry (ESI-MS). In the in vitro studies, Aca.B exhibited negligible toxicity and showed a dose-dependent nitric oxide inhibitory potential in Lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. In the in vivo studies, the oral administration of Aca.B to mice showed enhanced bioavailability and dose-dependent repression of the behavioral/cognitive impairment by regulating the cholinergic function, restoring the antioxidant status, attenuating the inflammatory cytokines/mediators and actively enriching neurotropic proteins in the hippocampal regions of the scopolamine-administered mice.



中文翻译:

通过调节氧化/炎症/胆碱能系统和激活TrkB / CREB ​​/ BDNF途径,刺五加酚B在东mouse碱诱导的失忆小鼠模型中的认知增强和改善作用

最近,我们的研究小组报告了欧洲Salalornia europaea L.(SE-EE)脱盐的氢乙醇提取物的抗记忆潜力。在这项研究中,我们从SE-EE中进行了生物活性指导的分离和鉴定Acanthoside B(Aca.B)作为潜在的生物活性候选物,并使用体内模型研究了其潜在作用机制的抗记忆删除活性。从SE-EE纯化的S7-L3-3显示增强的体外乙酰胆碱酯酶(AChE)抑制活性。使用各种光谱分析,即核磁共振(NMR),紫外-可见(UV-Vis)和电喷雾电离质谱(ESI-MS),鉴定出了分离的S7-L3-3并将其表征为Aca.B。在体外研究表明,Aca.B在脂多糖(LPS)刺激的B​​V-2小胶质细胞中表现出微不足道的毒性,并显示出剂量依赖性一氧化氮抑制潜能。在体内研究中,口服Aca.B通过调节胆碱能功能,恢复抗氧化剂状态,减弱炎性细胞因子/介体并积极丰富神经活性,从而增强了生物利用度并抑制了行为/认知障碍的剂量依赖性抑制作用东pol碱施用的小鼠海马区中的蛋白。

更新日期:2019-05-08
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