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首页> 外文期刊>Frontiers in Neuropharmacology >Facilitating Granule Cell Survival and Maturation in Dentate Gyrus With Baicalin for Antidepressant Therapeutics
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Facilitating Granule Cell Survival and Maturation in Dentate Gyrus With Baicalin for Antidepressant Therapeutics

机译：用黄芩苷促进颗粒细胞存活和成熟，用黄芩苷进行抗抑郁治疗

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Baicalin isolated from Scutellaria baicalensis possesses antidepressant abilities through its relation to hippocampal neurogenesis. Current research has found that baicalin can promote the proliferation of hippocampal granule cells, however, the detailed mechanism of baicalin on the survival and maturation of hippocampal granule cells has yet to be sufficiently explored. The purpose of this study was to evaluate whether baicalin could facilitate the survival and maturation of hippocampal granule cells, and to explore its potential mechanism. The chronic corticosterone (CORT)-induced mouse model of depression was used to assess antidepressant-like effects of baicalin and to illuminate possible molecular mechanisms by which baicalin affects hippocampal neurogenesis. The survival and maturation of granule cells were measured by immunohistochemistry, immunofluorescence and Golgi staining. The expression of Phosphatidylinositol 3-kinase (PI3K)/Protein kinase B (AKT)/glycogen synthase kinase-3β (GSK3β)/β-catenin pathway related proteins were measured by western blot analysis. PI3K inhibitor LY292002 and AKT inhibitor Perifosine were administered to HT-22 cells to explore the relationship between the PI3K/AKT/GSK3β/β-catenin pathway and baicalin. The results of the study illustrated that baicalin significantly decreased chronic CORT-induced depressive-like behaviors and reduced serum corticosterone levels. In addition, baicalin (administered at 60 mg/kg) reversed chronic CORT-induced lesions on hippocampal granule cells. Moreover, baicalin significantly increased the phosphorylation rate of PI3K, AKT, GSK3β, and total β-catenin. The study found that administration of LY292002/Perifosine counteracted the effects of baicalin in HT-22 cells. These results demonstrate that baicalin can alleviate chronic CORT-induced depressive-like behaviors through promoting survival and maturation of adult-born hippocampal granule cells and exhibiting protective effect on hippocampal neuron morphology. We propose the underlying mechanisms involve the activation of the PI3K/AKT/GSK3β/β-catenin pathway.
机译：来自Scutellaria Baicalensis的黄芩苷通过其与海马神经发生的关系具有抗抑郁能力。目前的研究发现，黄芩苷可以促进海马颗粒细胞的增殖，然而，黄芩苷对海马颗粒细胞的存活和成熟的详细机制尚未得到充分探索。本研究的目的是评估黄芩苷是否可以促进海马颗粒细胞的存活率和成熟，并探讨其潜在机制。慢性皮质酮（皮质）抑制的抑郁小鼠模型用于评估黄芩苷的抗抑郁作用，并照亮BACICALIN影响海马神经发生的可能的分子机制。通过免疫组织化学，免疫荧光和高尔基染色测量颗粒细胞的存活率和成熟。通过蛋白质印迹分析测量磷脂酰肌醇3-激酶（PI3K）/蛋白激酶-3β（GSK3β）/β-Catenin途径相关蛋白质的表达。将PI3K抑制剂LY292002和AKT抑制剂杂化物施用于HT-22细胞，探讨PI3K / AKT / GSK3 /β-连环蛋白途径和黄芩苷之间的关系。研究结果表明，黄芩苷显着降低了慢性皮质诱导的抑郁型行为和减少血清皮质酮水平。此外，黄芩苷（以60mg / kg施用）逆转慢性皮质诱导的海马颗粒细胞病变。此外，黄芩苷显着提高了PI3K，AKT，GSK3β和总β-Catenin的磷酸化率。该研究发现，Ly292002 / perifosine的给药抵消了黄芩苷在HT-22细胞中的影响。这些结果表明，通过促进成人出生的海马颗粒细胞的存活和成熟并对海马神经元形态表现出保护作用，可以缓解慢性皮质诱导的抑郁症行为。我们提出了潜在的机制涉及激活PI3K / AKT /GSK3β/β-连环蛋白途径。

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