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Abstract Title:

The antidepressant effects of hesperidin on chronic unpredictable mild stress-induced mice.

Abstract Source:

Eur J Pharmacol. 2019 Mar 27. Epub 2019 Mar 27. PMID: 30928632

Abstract Author(s):

Huiling Fu, Li Liu, Yue Tong, Yuanjie Li, Xia Zhang, Xiaojuan Gao, Jingjiao Yong, Jianjun Zhao, Dong Xiao, Kuishen Wen, Hanqing Wang

Article Affiliation:

Huiling Fu

Abstract:

Hesperidin, a kind of citrus bioflavonoid distributed in foods including grapefruits, oranges and lemons, has many pharmacological activities. This study was aimed to evaluate the anti-depressant-like effect of hesperidin on chronic unpredictable mild stress (CUMS)-induced mice. Depressive-like behavior was detected by the sucrose preference test (SPT), tail suspension test (TST) and forced swimming test (FST). A 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was performed to assess the cell viability of corticosterone-induced PC12 cells. The serum, hippocampal and cell supernatant concentrations of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α were determined using enzyme-linked immunosorbent assay (ELISA) commercial kits. Furthermore, the protein expression levels of high-mobility group box 1 protein (HMGB1), receptor for advanced glycation end-products (RAGE)/NF-κB and brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) pathway in the hippocampus and corticosterone-induced PC12 cells were detected by Western blot. Our results showed that hesperidin (100, 200 mg/kg) significantly relieved depressive-like behaviors, including decreased sucrose consumption in sucrose preference test (SPT), immobility in the forced swimming test (FST), tail suspension test, and locomotor activity in the open field test (OFT). Hesperidin reduced inflammatory cytokine levels by attenuating the HMGB1/RAGE/NF-κB signaling pathway and BDNF/TrkB pathway both in vivo and in vitro. In conclusion, hesperidin possessed efficient neuroprotective effects on depression, which was associated with neuroinflammation mediated by the HMGB1/RAGE/NF-κB and BDNF/TrkB pathways.

Study Type : Animal Study, In Vitro Study

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