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Asarones 从 Acori Tatarinowii Rhizoma 刺激神经营养因子在培养的星形胶质细胞中的表达和分泌。

Asarones from Acori Tatarinowii Rhizoma stimulate expression and secretion of neurotrophic factors in cultured astrocytes.

机构信息

Division of Life Science and Center for Chinese Medicine, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China.

Shenzhen Key Laboratory of Edible and Medicinal Bioresources, Shenzhen Research Institute, Hi-Tech Park, Nanshan, Shenzhen, 518000, China.

出版信息

Neurosci Lett. 2019 Aug 10;707:134308. doi: 10.1016/j.neulet.2019.134308. Epub 2019 May 31.

Abstract

Acori Tatarinowii Rhizoma (ATR, the dried rhizome of Acorus tatarinowii Schott.) is a traditional Chinese medicine widely used to treat brain diseases, e.g. depression, forgetfulness, anxiety and epilepsy. Several lines of evidence support that ATR has neuronal beneficial functions in animal models, but its action mechanism in cellular level is unknown. Here, we identified α-asarone and β-asarone could be the major active ingredients of ATR, which, when applied onto cultured rat astrocytes, significantly stimulated the expression and secretion of neurotrophic factors, i.e. nerve growth factor (NGF), brain derived neurotrophic factor (BDNF) and glial derived neurotrophic factor (GDNF), in dose-dependent manners. These results suggested that the neuronal action of ATR, triggered by asarone, might be mediated by an increase of expression of neurotrophic factors in astrocytes, which therefore could support the clinical usage of ATR. In addition, application of PKA inhibitor, H89, in cultured astrocytes partially blocked the asarone-induced neurotrophic factor expression, suggesting the involvement of PKA signaling. The results proposed that α-asarone and β-asarone from ATR could serve as potential candidates for drug development in neurodegenerative diseases.

摘要

石菖蒲(ATR,石菖蒲的干燥根茎)是一种传统的中药,广泛用于治疗脑部疾病,如抑郁症、健忘症、焦虑症和癫痫。有几条证据表明 ATR 在动物模型中具有神经元有益功能,但它在细胞水平上的作用机制尚不清楚。在这里,我们鉴定出α-细辛脑和β-细辛脑可能是 ATR 的主要活性成分,当应用于培养的大鼠星形胶质细胞时,它们以剂量依赖的方式显著刺激神经营养因子(NGF、BDNF 和 GDNF)的表达和分泌。这些结果表明,ATR 通过细辛脑触发的神经元作用可能是通过星形胶质细胞中神经营养因子表达的增加来介导的,因此可以支持 ATR 的临床应用。此外,在培养的星形胶质细胞中应用 PKA 抑制剂 H89 部分阻断了细辛脑诱导的神经营养因子表达,表明 PKA 信号的参与。结果表明,ATR 中的α-细辛脑和β-细辛脑可以作为神经退行性疾病药物开发的潜在候选药物。

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