• Lianjin Weng, Xiaohua Guo, Yang Li, Xin Yang, and Yuanyuan Han.
• Department of Chemical and Pharmaceutical Engineering, College of Chemical Engineering, Huaqiao University, No. 668, Jimei Road, Xiamen, Fujian Province, PR China. Electronic address: lianjin.weng@yahoo.com.
• Eur. J. Pharmacol. 2016 Mar 5; 774: 50-4.

AbstractPrevious researches found that apigenin exerted antidepressant-like effects in rodents. However, it is unclear whether the neurotrophic system is involved in the antidepressant-like effects of apigenin. Our present study aimed to explore the neurotrophic related mechanism of apigenin in depressive-like mice induced by chronic corticosterone treatment. Mice were repeatedly injected with corticosterone (40 mg/kg) subcutaneously (s.c) once daily for consecutive 21 days. Apigenin (20 and 40 mg/kg) and fluoxetine (20 mg/kg) were administered 30 min prior to the corticosterone injection. The behavioral tests indicated that apigenin reversed the reduction of sucrose preference and the elevation of immobility time in mice induced by chronic corticosterone treatment. In addition, the increase in serum corticosterone levels and the decrease in hippocampal brain-derived neurotrophic factor (BDNF) levels in corticosterone-treated mice were also ameliorated by apigenin administration. Taken together, our findings intensively confirmed the antidepressant-like effects of apigenin and indicated that the antidepressant-like mechanism of apigenin was mediated, at least partly by up-regulation of BDNF levels in the hippocampus.Copyright © 2016 Elsevier B.V. All rights reserved.

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