Abstract
Amyloid-β (Aβ) accumulation is one of the main pathological hallmarks of Alzheimer’s disease (AD). Porphyromonas gingivalis (P. gingivalis), the pathogen of chronic periodontitis, could cause Aβ accumulation and was identified in the brain of AD patients. Salvianolic Acid B (SalB) has been proven to have the neuroprotective effect. Whether SalB could protect against P. gingivalis-induced cognitive impairment is still unknown. In this study, a P. gingivalis-infected mouse model was employed to study the neuroprotective role of SalB. The results showed that SalB (20 and 40 mg/kg) treatment for 4 weeks could shorten the escape latency and improve the percentage of spontaneous alternation in the P. gingivalis-infected mice. SalB inhibited the levels of reactive oxygen species and malondialdehyde, while increased the levels of antioxidative enzymes (superoxide dismutase and glutathione peroxidase). SalB decreased the levels of IL-1β and IL-6, increased the mRNA levels of bdnf and ngf in the brain of P. gingivalis-infected mice. In addition, SalB obviously decreased the level of Aβ. SalB elevated the protein expression of ADAM10, while downregulated BACE1 and PS1. SalB increased the protein expression of LRP1, while decreased RAGE. In conclusion, SalB could improve cognitive impairment by inhibiting neuroinflammation and decreasing Aβ level in P. gingivalis-infected mice.
Highlights
Sleep is a fundamental conserved physiological process of the human body, and the quality and quantity of sleep can affect individual health status and quality of life [1]
We found that the potential molecular mechanism for the effects of Ellagic acid (EA) versus sleep deprivation (SD) was related to the modulation of TLR4 and Nuclear factor erythroid 2-related factor 2 (Nrf2)
Consistent with the behavioral data in our study and others, EA had a normalizing effect on www.aging-us.com the levels of proinflammatory cytokines and oxidative stress parameters in the hippocampus of SD mice
Summary
Sleep is a fundamental conserved physiological process of the human body, and the quality and quantity of sleep can affect individual health status and quality of life [1]. It has been well documented that inadequate sleep is detrimental to human health [4, 5]. Sleep deprivation has long been known to impair neurobehavior. This cognitive function impairment is related to increased oxidative stress and inflammation in the brain. Glu generates oxidative stress by various mechanisms, which leads to increased reactive oxygen species (ROS) production. The abnormal production of ROS causes oxidation of biological macromolecules and the expression of inflammatory mediators and genes, leading to an increase in the risk of neurodegenerative diseases
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