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Effect of red chicory extract on scopolamine-induced memory impairment in mice

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We investigated the protective effects and mechanisms of red chicory extract (RCE) on scopolamine-induced memory impairment in mice. Antioxidant effects were investigated by measuring DPPH radical scavenging activity, and cell viability and intracellular ROS levels were examined by inducing cytotoxicity with L-glutamate in HT-22 cells. In addition, mice were administered orally with RCE (150 and 300 mg/kg). Memory was evaluated using Morris water maze (MWZ) and passive avoidance tests. Administration of SRCE 150 kg/mg significantly increased escape latency time (p<0.05) that was shortened by scopolamine. It further increased platform crossing numbers after 7 days of training in MWZ tests (p<0.05), which were significantly shortened by scopolamine, and prolonged latency (p<0.01) in passive avoidance tests. Biochemical findings showed significantly increased total glutathione (GSH) (p<0.05), glutathione S-transferase (GST) (p<0.01), and glutathione peroxidase (GPx) (p<0.01) in the mice administered RCE 150 mg/kg compared with the scopolamine-induced positive control. Glutathione reductase (GR) did not significantly differ between the RCE 300 mg/kg and scopolamine-induced groups (p<0.05). These results suggested that RCE has antioxidant activity and enhances scopolamine-induced cognitive impairment by attenuating oxidative stress.

Abstract

We investigated the protective effects and mechanisms of red chicory extract (RCE) on scopolamine-induced memory impairment in mice. Antioxidant effects were investigated by measuring DPPH radical scavenging activity, and cell viability and intracellular ROS levels were examined by inducing cytotoxicity with L-glutamate in HT-22 cells. In addition, mice were administered orally with RCE (150 and 300 mg/kg). Memory was evaluated using Morris water maze (MWZ) and passive avoidance tests. Administration of SRCE 150 kg/mg significantly increased escape latency time (p<0.05) that was shortened by scopolamine. It further increased platform crossing numbers after 7 days of training in MWZ tests (p<0.05), which were significantly shortened by scopolamine, and prolonged latency (p<0.01) in passive avoidance tests. Biochemical findings showed significantly increased total glutathione (GSH) (p<0.05), glutathione S-transferase (GST) (p<0.01), and glutathione peroxidase (GPx) (p<0.01) in the mice administered RCE 150 mg/kg compared with the scopolamine-induced positive control. Glutathione reductase (GR) did not significantly differ between the RCE 300 mg/kg and scopolamine-induced groups (p<0.05). These results suggested that RCE has antioxidant activity and enhances scopolamine-induced cognitive impairment by attenuating oxidative stress.

참고문헌 (23)

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