首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Asarones from Acori Tatarinowii Rhizoma stimulate expression and secretion of neurotrophic factors in cultured astrocytes
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Asarones from Acori Tatarinowii Rhizoma stimulate expression and secretion of neurotrophic factors in cultured astrocytes

机译:来自Acori Tatarinowii神的asarones刺激培养星形胶质细胞中神经营养因子的表达和分泌

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摘要

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 alpha-asarone and beta-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 alpha-asarone and beta-asarone from ATR could serve as potential candidates for drug development in neurodegenerative diseases.
机译:Acori Tatarinowii噻嗪(ATR,Acorus Tatarinowii Schott的干根茎)是一种中国中药,广泛用于治疗脑病,例如脑疾病。抑郁症,健忘,焦虑和癫痫。若干证据支持,ATR在动物模型中具有神经元有益功能,但其在细胞层中的动作机制是未知的。在这里,我们鉴定了α-asarone和β-asarone可以是ATR的主要活性成分,当施用于培养的大鼠星形胶质细胞时,显着刺激神经营养因子的表达和分泌,即神经生长因子(NGF),脑衍生的神经营养因子(BDNF)和神经胶质衍生的神经营养因子(GDNF),以剂量依赖的方式。这些结果表明,ATR的神经元作用可以通过增加星形胶质细胞的神经营养因子表达的增加来介导,因此可以支持ATR的临床使用。此外,在培养的星形胶质细胞中施加PKA抑制剂H89,部分阻断了咸诱导的神经营养因子表达,表明PKA信号传导的累及。结果提出,来自ATR的α-珊瑚酮和β-亚辛酮可以作为神经变性疾病中药物发育的潜在候选者。

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