Daidzein黄豆苷元,486-66-8

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Daidzein

CAS No. : 486-66-8

MCE 国际站：Daidzein

产品活性：Daidzein 是一种大豆异黄酮，可用作 PPAR 激活剂。

研究领域：Cell Cycle/DNA Damage | Metabolic Enzyme/Protease

作用靶点：PPAR | Endogenous Metabolite

结构分类：酚类 | 多酚类 | 黄酮类 | 异黄酮

来源：植物 | 豆科 | 大豆

In Vitro: In 3T3-L1 adipocytes, Daidzein inverses the attenuation of adiponectin gene expression by co-culture, and these effects are inhibited by the PPAR-γ specific inhibitor. Daidzein attenuates the reduction of adiponectin expression in adipocytes, and a PPAR-γ specific inhibitor abrogated this effect. Direct activation of PPAR-α and-γ by Daidzein is confirmed by a luciferase reporter assay. In HEK293T cells, Daidzein significantly increases PPAR-α transcriptional activity in a concentration-dependent manner. Although an obvious dose-dependency is not observed in PPAR-γ transcriptional activity, Daidzein also significantly increases PPAR-γ transcriptional activity over a similar range of concentrations at which Daidzein enhanced PPAR-α transcriptional activity, with a maximum increase at 25 μM. Daidzein is a soy isoflavone, which upregulates the expression of Abcg1, and it promotes axonal outgrowth in cultured hippocampal neurons via estrogen receptor signaling. Daidzein is a major component of soy with structural similarity to estrogen. It exerts an anti-inflammatory effect, lowers lipid levels, and increases mitochondrial biogenesis. As an activator of nuclear receptor peroxisome proliferator-activated receptors (PPARs), Daidzein enhances transcription of PPARs-dependent genes, including liver X receptors (LXRs, Nr1h gene family in mice). Incubation with different concentrations of Daidzein, from 5 to 100 μM, increases APOE transcriptional activity.

In Vivo: Treating Apoe KO mice with Daidzein increases Lxr and Abca1 gene expression at 1 month after stroke, showing that the absence of ApoE does not interfere with other cholesterol homeostasis genetic programs. Therefore, the findings suggest that Daidzein-induced ApoE upregulation is a critical component in fostering functional recovery in chronic stroke.

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