Ginsenoside Rg1 reverses stress-induced depression-like behaviours and brain-derived neurotrophic factor expression within the prefrontal cortex
Ginsenoside Rg1 reverses stress-induced depression-like behaviours and brain-derived neurotrophic factor expression within the prefrontal cortex
复制标题
人参皂苷 Rg1 逆转压力诱发的抑郁样行为和前额皮质内脑源性神经营养因子的表达
DOI：
10.1111/ejn.13255
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发表时间：
2016
影响因子：
3.4
通讯作者：
Yu Shu Yan
中科院分区：
文献类型：
--
作者：
Zhu Xiuzhi;Gao Rui;Liu Zhuxi;Cheng Ziyi;Qi Yihang;Fan Cuiqin;Yu Shu Yan
抑郁症是一种主要的神经精神疾病，对公众健康产生有害影响。然而，抑郁症的神经元机制仍然在很大程度上未被表征，这阻碍了用于治疗这种疾病的有效治疗工具的识别和开发。本研究的目的是探索人参皂苷Rg 1（一种在人参中发现的天然甾体皂苷）对慢性应激诱导的抑郁症的保护作用的神经机制。5周）显著改善大鼠的抑郁样行为，如在蔗糖偏好和强迫游泳试验中所评估的。此外，慢性应激降低了前额叶皮层细胞外信号调节激酶和cAMP反应元件结合蛋白的磷酸化水平，并导致脑源性神经营养因子表达减少。特别重要的是，这些参数的所有降低均通过预先给予Rg 1显著逆转。综上所述，本研究的结果表明，EARRg 1的抗抑郁样作用可能是通过激活前额叶皮层内的cAMP反应元件结合蛋白-脑源性神经营养因子系统介导的，至少部分是通过激活前额叶皮层内的cAMP反应元件结合蛋白-脑源性神经营养因子系统介导的。这些发现不仅揭示了抑郁症的一些潜在的神经机制，而且还揭示了Rg 1作为预防剂在治疗抑郁症中的治疗潜力。
Depression is a major neuropsychiatric disorder that exerts deleterious effects upon public health. However, the neuronal mechanisms of depression remain largely uncharacterized, which has retarded the identification and development of effective therapeutic tools for the treatment of this disorder. The aim of this study was to explore the neuronal mechanisms underlying the protective effects of ginsenoside Rg1, a natural steroidal saponin found in ginseng, against chronic stress‐induced depression.The results showed that chronic administration of ginsenoside Rg1 (40 mg/kg, i.p., 5 weeks) significantly ameliorated depression‐like behaviours in rats as assessed in the sucrose preference and forced swim tests. Furthermore, chronic stress decreased the phosphorylation levels of the extracellular signal‐regulated kinase and cAMP‐response element‐binding protein in the prefrontal cortex as well as producing a reduction of brain‐derived neurotrophic factor expression. Of particular importance, all reductions in these parameters were significantly reversed by pre‐treatment with ginsenoside Rg1. Taken together, the results of the present study suggest that the antidepressant‐like effect of ginsenoside Rg1 might be mediated, at least in part, by activating the cAMP‐response element‐binding protein–brain‐derived neurotrophic factor system within the prefrontal cortex. These findings not only reveal some of the underlying neuronal mechanisms of depression, but also the therapeutic potential of ginsenoside Rg1 as a preventive agent in the treatment of depression.