Quercetin mitigates depression-like behavior via the suppression of neuroinflammation and oxidative damage in corticosterone-induced mice

行为绝望测验 槲皮素 内分泌学 开阔地 内科学 皮质酮 海马体 神经炎症 高架加迷宫 化学 药理学 心理学 医学 抗氧化剂 抗抑郁药 生物化学 炎症 激素 精神科 焦虑
作者
Chenjie Ge,Shiliang Wang,Xuqi Wu,Lilei Lei
出处
期刊:Journal of Chemical Neuroanatomy [Elsevier]
卷期号:132: 102313-102313 被引量:21
标识
DOI:10.1016/j.jchemneu.2023.102313
摘要

Depression is a clinically common and easily overlooked mental disease. Quercetin is a flavonoid compound, which has anti-inflammatory and antioxidant roles. Previous reports presented the anti-depressant role of quercetin. Nevertheless, the latent mechanism of the anti-depressant function of quercetin is blurry. This research aimed to probe its effects on corticosterone (CORT)-induced depression-like behaviors and explore the underlying mechanism. A depression model was established by subcutaneous injection of CORT (20 mg/kg). Thereafter, CORT-treated mice were given 40 mg/kg and 80 mg/kg of quercetin by gavage. This study found that quercetin mitigated depression-like behaviors, as evidenced by increased the number of line crossings, swimming time, and time spent in open arm and reduced thigmotaxis time in CORT-challenged mice in open field test and decreased immobility time as well as the swimming and climbing time in forced swim test and increased number of head dips, time spent and entries in open arm elevated plus maze test. Also, quercetin exerted anti-inflammatory and anti-oxidation effects in hippocampus and prefrontal cortex of CORT-induced mice. Additionally, quercetin alleviated the pathological injury of the liver tissue and weakened alkaline phosphatase (ALP) and alanine aminotransferase (ALT) concentrations of the serum in CORT-induced mice. Quercetin also suppressed Caspase-3 content but advanced vascular endothelial growth factor (VEGF) and brain derived neurotrophic factor (BDNF) contents in hippocampus of CORT-treated mice. Based on these results, quercetin mitigated CORT-induced depression-like behaviors, and the mechanism was partly related to the repression of neuroinflammation and oxidative damage.

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