Journal
METABOLIC BRAIN DISEASE
Volume 31, Issue 4, Pages 771-778Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11011-016-9813-2
Keywords
Sal; Aging; Cognitive impairment; Neuroinflammation; SIRT1/NF-kappa B pathway
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Funding
- National twelve five major drug discovery project [2011ZX09102-002-01]
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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-kappa B) 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-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). Moreover, D-gal-induced activation of NF-kappa B 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-kappa B signaling pathway, whereas treatment with Sal could positively affect these changes in hippocampus.
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