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红景天苷通过SIRT1/NF-κB信号通路抑制D-半乳糖诱导的大鼠阿尔茨海默病模型中的炎症反应。

Salidroside suppresses inflammation in a D-galactose-induced rat model of Alzheimer's disease via SIRT1/NF-κB pathway.

作者信息

Gao Jin, Zhou Rui, You Xintong, Luo Fen, He He, Chang Xiayun, Zhu Lingpeng, Ding Xuansheng, Yan Tianhua

机构信息

Department of Physiology and Pharmacology, China Pharmaceutical University, Nanjing, 210009, China.

Department of Polymer Materials and Engineering, Nanjing Forestry University, Nanjing, 210037, China.

出版信息

Metab Brain Dis. 2016 Aug;31(4):771-8. doi: 10.1007/s11011-016-9813-2. Epub 2016 Feb 24.

Abstract

Age-related inflammation is the predominant factor for neurodegenerative diseases like Alzheimer's disease (AD). In the present study, we examined memory performance and neuroinflammation in D-galactose (D-gal)-induced sub-acute aging model of rats. Our results demonstrated that chronic administration of D-gal (120 mg/kg) produced cognitive impairment as determined by Morris water maze (MWM) test and step-down passive avoidance test. D-gal also activated nuclear factor kappa B (NF-κB) p65/RelA by down-regulating the expression level of sirtuins 1 (SIRT1) in the hippocampus. Treatment with Salidroside (Sal, 20, 40 mg/kg) for 28 days ameliorated D-gal-induced memory deficits and inflammatory mediators including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Moreover, D-gal-induced activation of NF-κB signaling pathway in the brain was also inhibited by Sal via up-regulating SIRT1. These results suggest that D-gal-triggered memory impairment and inflammatory response may be associated with SIRT1/NF-κB signaling pathway, whereas treatment with Sal could positively affect these changes in hippocampus.

摘要

与年龄相关的炎症是诸如阿尔茨海默病(AD)等神经退行性疾病的主要因素。在本研究中,我们检测了D-半乳糖(D-gal)诱导的大鼠亚急性衰老模型中的记忆表现和神经炎症。我们的结果表明,通过莫里斯水迷宫(MWM)试验和被动回避试验确定,长期给予D-半乳糖(120mg/kg)会导致认知障碍。D-半乳糖还通过下调海马中沉默调节蛋白1(SIRT1)的表达水平来激活核因子κB(NF-κB)p65/RelA。用红景天苷(Sal,20、40mg/kg)治疗28天可改善D-半乳糖诱导的记忆缺陷以及包括肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)在内的炎症介质。此外,Sal通过上调SIRT1抑制了D-半乳糖诱导的大脑中NF-κB信号通路的激活。这些结果表明,D-半乳糖引发的记忆损伤和炎症反应可能与SIRT1/NF-κB信号通路有关,而Sal治疗可对海马中的这些变化产生积极影响。

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