Abstract
The present study was designed to find out the initial factor that triggered cognitive deficits induced by high-fat diets (HFD) and whether salvianolic acid B (Sal B) had beneficial role on cognition. Seven weeks' consumption of HFD resulted in higher food intake, dyslipidaemia, cognitive impairment and increasing hippocampal and frontal cortex oxidative stress (OS) without significant change in blood glucose and hippocampal inflammation. Microarray analysis data demonstrated that long-term potentiation (LTP) pathway was altered with down-regulation of genes against OS. Correlation analysis showed that hippocampal OS biomarkers had strong relations to Morris water maze performance. Sal B in drinking water (0.07 mg/ml) normalised the cognitive deficits through attenuating hippocampal redox status, altering LTP pathway and other biological pathways, up-regulating antioxidative genes expression. Thus, OS induced by HFD might be the initial factor that triggers cognitive impairment. Sal B was an efficient agent that exerted neuroprotective effects.
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