A UPLC-Q/TOF-MS-based plasma and hippocampal metabolomics analysis was conducted to investigate the impact of Erjing Pills on Alzheimer's Disease rats.

Abstract

Alzheimer's Disease (AD), the most common form of dementia, places a significant burden on individuals and society. In line with the doctrines of Chinese medical practice, kidney deficiency and insufficient marrow cannot nourish the brain, leading to insufficient blood, cerebral dysfunction, and ultimately dementia. Erjing Pills contain wolfberry and Polygonati Rhizoma, which tonify the kidneys and improve the essence. Although pharmacological studies have demonstrated that Erjing Pills can be used to prevent and treat AD, the detailed action mechanism is yet to be determined. To comprehensively reveal the mechanism of action of Erjing Pills in the prevention and treatment of AD, three pharmacodynamic evaluations, the water maze test, both hematoxylin-eosin and immunohistochemical techniques were utilized to assess the effects of Erjing Pills on AD rats. Furthermore, plasma and hippocampus metabolomics were conducted by various statistical analyses combined with UPLC-Q/TOF-MS were employed for a comprehensive and accurate analysis of the in vivo anti-AD effects of Erjing Pills. Erjing Pills enhanced learning and memory capacity decreased hippocampal Aβ deposition expression, and enhanced hippocampal morphology in AD rats. After Erjing Pills treatment, 38 plasma metabolites and 15 hippocampal metabolites of AD rats were regressed to levels similar to those of controls. Moreover, pathways impacted by Erjing Pills on AD included arachidonic acid metabolism, retinol metabolism, glycerophospholipid metabolism, and caffeine metabolism. Additionally, adrenaline, leukotriene B4, retinol, and paraxanthine clearly distinguished the Erjing Pills group from the AD group. These findings significantly enhance our comprehension of the metabolic pathways implicated in AD and shed light on the therapeutic mechanisms of Erjing Pills in alleviating symptoms in rats with AD.