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黄芩苷降低海马中血清糖皮质激素诱导激酶1(SGK1)的表达,并逆转皮质酮诱导的抑郁样行为。

Baicalin decreases SGK1 expression in the hippocampus and reverses depressive-like behaviors induced by corticosterone.

作者信息

Li Y-C, Wang L-L, Pei Y-Y, Shen J-D, Li H-B, Wang B-Y, Bai M

机构信息

College of Pharmacy, Henan University of Traditional Chinese Medicine, Zhengzhou 450046, PR China.

College of Pharmacy, Henan University of Traditional Chinese Medicine, Zhengzhou 450046, PR China.

出版信息

Neuroscience. 2015 Dec 17;311:130-7. doi: 10.1016/j.neuroscience.2015.10.023. Epub 2015 Oct 19.

DOI:10.1016/j.neuroscience.2015.10.023
PMID:26480816
Abstract

The present study was to investigate whether baicalin can prevent repeated exogenous corticosterone injection-induced depressive-like behaviors and explore its possible mechanisms. After a 21-day treatment with baicalin (10 and 20 mg/kg), sucrose preference in the sucrose preference test (SPT) and immobility time in forced swimming test (FST) were observed, serum corticosterone levels and brain-derived neurotrophic factor (BDNF) contents in the hippocampus were examined by enzyme-linked immunosorbent assay (ELISA). In addition, quantitative real-time polymerase chain reaction (qPCR) and western blot were used to detect the mRNA and protein expression in the hippocampus. The results showed that 21-day cortiscosterone injections caused depressive-like behaviors in mice, including the reduced sucrose preference and increased duration of immobility. Baicalin reversed these behavioral changes described above and restored serum corticosterone levels. Additionally, baicalin up-regulated the mRNA and protein expression of glucocorticoid receptor (GR) and BDNF, accompanied with the down-regulation of serum- and glucocorticoid-regulated kinase 1 (SGK1) in the hippocampus. Moreover, baicalin significantly increased the protein expression of 11β-hydroxysteroid dehydrogenase-2 (11β-HSD2) in the hippocampus. The present results confirmed the antidepressant-like effects of baicalin in a mice model of depression induced by corticosterone and suggested that its mechanism was possibly involved in reducing serum corticosterone and thereby increasing BDNF in the hippocampus.

摘要

本研究旨在探讨黄芩苷是否能预防反复注射外源性皮质酮诱导的抑郁样行为,并探究其可能的机制。用黄芩苷(10和20mg/kg)治疗21天后,观察蔗糖偏好试验(SPT)中的蔗糖偏好和强迫游泳试验(FST)中的不动时间,采用酶联免疫吸附测定(ELISA)检测血清皮质酮水平和海马中脑源性神经营养因子(BDNF)含量。此外,采用定量实时聚合酶链反应(qPCR)和蛋白质免疫印迹法检测海马中的mRNA和蛋白表达。结果显示,连续21天注射皮质酮可导致小鼠出现抑郁样行为,包括蔗糖偏好降低和不动时间延长。黄芩苷可逆转上述行为变化,并恢复血清皮质酮水平。此外,黄芩苷上调海马中糖皮质激素受体(GR)和BDNF的mRNA和蛋白表达,同时下调血清和糖皮质激素调节激酶1(SGK1)。此外,黄芩苷显著增加海马中11β-羟基类固醇脱氢酶-2(11β-HSD2)的蛋白表达。本研究结果证实了黄芩苷在皮质酮诱导的小鼠抑郁模型中的抗抑郁样作用,并提示其机制可能与降低血清皮质酮从而增加海马中BDNF有关。

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