Journal
MOLECULAR NUTRITION & FOOD RESEARCH
Volume 67, Issue 11, Pages -Publisher
WILEY
DOI: 10.1002/mnfr.202200735
Keywords
chronic sleep deprivation; cognitive impairment; Farnesol; oxidative stress; Sirt1; Nrf2 signaling pathway
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This study demonstrates that farnesol (FOL) can protect against cognitive impairment caused by sleep deprivation (SD) through activation of the Sirt1/Nrf2 signaling pathway.
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.
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