Farnesol Exerts Protective Effects against Chronic Sleep Deprivation‐Induced Cognitive Impairment via Activation SIRT1/Nrf2 Pathway in the Hippocampi of Adult Mice

Abstract

ScopeSleep deprivation (SD) negatively affects all aspects of health, with one serious consequence being impaired cognition. Farnesol (FOL) is a sesquiterpene synthesized by plants and mammals that has antioxidant, anti‐inflammatory, and neuroprotective properties. This study investigates the mechanism underlying the neuroprotective effect of FOL on SD‐induced cognitive impairment.Methods and resultsAdministration of FOL dramatically ameliorates chronic sleep deprivation (CSD)‐induced cognitive impairment. In addition, FOL notably attenuates oxidative stress damage, pro‐inflammatory cytokines activation, and microglial activation in the hippocampi of the CSD‐exposed mice. Further examination indicates that administration of FOL after the CSD significantly increases the protein expressions of silent information regulator factor 2‐related enzyme 1 (Sirt1), nuclear factor erythroid 2‐related factor 2 (Nrf2), heme oxygenase‐1 (HO‐1), and glutathione peroxidase 4 (Gpx4) in the hippocampi. Sirt1 agonist resveratrol (RES) has a similar neuroprotective effect, indicating that FOL could exert neuroprotective effects through the activation of the Sirt1/Nrf2 signaling pathway.ConclusionThe results reveal that FOL could protect against CSD‐induced cognitive impairment by activating the Sirt1/Nrf2 signaling pathway.