Objective: Anesthesia-induced cognitive impairments are common for elder patients after surgery. Oxidative stress is the predominant factor contributing to the impairments. This study was to assess the therapeutic potential of an anti-oxidative naturally occurring flavonoid, chrysin, in attenuating sevoflurane-induced cognitive impairments in rat models. Methods: Rat models of cognitive impairments were constructed by exposing aged rats (18 months old) to sevoflurane for 2 h. Chrysin was administered via oral gavage at the dose of 25, 50, and 100 mg/kg/day for seven days. The elevated plus maze test was used to assess anxiety and explorative behaviors. Spatial memory tests were performed using novel object recognition test, object location memory task, and water maze experiments. Oxidative stress was evaluated by measuring levels of malondialdehyde, nicotinamide adenine dinucleotide phosphate, 4-hydroxynonenal, and glutathione using colorimetric assays. Quantitative real-time polymerase chain reaction and Western blot were used to analyze how chrysin affects nuclear factor E2-related factor (Nrf) signaling. Results: While sevoflurane anesthesia led to significant decline in cognitive performance in object recognition test, object location memory task, and water maze test, chrysin exerted significant effects in alleviating the impairments. Oxidative stress was also reduced in the hippocampus tissue of rats after chrysin intake. Nrf signaling was activated by chrysin treatment in sevoflurane-induced cognitive impairment models. Conclusion: Chrysin was effective in alleviating cognitive impairments induced by sevoflurane anesthesia, which was at least in part facilitated by its effects in reducing oxidative stress via activating Nrf signaling.
Objective: Anesthesia-induced cognitive impairments are common for elder patients after surgery. Oxidative stress is the predominant factor contributing to the impairments. This study was to assess the therapeutic potential of an anti-oxidative naturally occurring flavonoid, chrysin, in attenuating sevoflurane-induced cognitive impairments in rat models. Methods: Rat models of cognitive impairments were constructed by exposing aged rats (18 months old) to sevoflurane for 2 h. Chrysin was administered via oral gavage at the dose of 25, 50, and 100 mg/kg/day for seven days. The elevated plus maze test was used to assess anxiety and explorative behaviors. Spatial memory tests were performed using novel object recognition test, object location memory task, and water maze experiments. Oxidative stress was evaluated by measuring levels of malondialdehyde, nicotinamide adenine dinucleotide phosphate, 4-hydroxynonenal, and glutathione using colorimetric assays. Quantitative real-time polymerase chain reaction and Western blot were used to analyze how chrysin affects nuclear factor E2-related factor (Nrf) signaling. Results: While sevoflurane anesthesia led to significant decline in cognitive performance in object recognition test, object location memory task, and water maze test, chrysin exerted significant effects in alleviating the impairments. Oxidative stress was also reduced in the hippocampus tissue of rats after chrysin intake. Nrf signaling was activated by chrysin treatment in sevoflurane-induced cognitive impairment models. Conclusion: Chrysin was effective in alleviating cognitive impairments induced by sevoflurane anesthesia, which was at least in part facilitated by its effects in reducing oxidative stress via activating Nrf signaling.
INTRODUCTION METHODS RESULTS DISCUSSIONS REFERENCES
