Abstract
Purpose: To investigate the effect of carnosol on the progression of postoperative cognitive dysfunction (POCD) and to elucidate its mechanism of action.
 Methods: A cognitive impairment model rat induced by sevoflurane (SEV) was established. Dihydroethidium (DHE) assay was conducted to determine the effect of carnosol on reactive oxygen species (ROS) levels in sevoflurane-induced rats. Adenosine triphosphate (ATP) production and immunoblot assays were used to assess carnosol effect on mitochondrial damage, while water maze experiment was performed to evaluate cognitive dysfunction in the rats. The mechanism of action was investigated using immunoblot assay.
 Results: Carnosol suppressed sevoflurane-induced ROS production in the rats, and alleviated sevoflurane-induced mitochondrial damage; it also activated autophagy. Furthermore, carnosol suppressed SEV-induced NLRP3 inflammasome activation by activating autophagy and suppressing SEV-induced cognitive dysfunction via the suppression of NLRP3 inflammasome activation.
 Conclusion: Carnosol ameliorates SEV-stimulated cognitive impairment by suppressing NLRP3 inflammasome and thus, can potentially be developed serve as a therapeutic agent for the management of cognitive impairment.
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