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Ginsenoside Re

CAS No. : 52286-59-6

MCE 国际站：Ginsenoside Re

产品活性：Ginsenoside Re (Ginsenoside B2) 是一种 Panax notoginseng 提取物。Ginsenoside Re 可降低 β-淀粉样蛋白 (Aβ)。Ginsenoside Re 还通过抑制 JNK 和 NF-κB 发挥抗炎作用。

研究领域：Neuronal Signaling  |  NF-κB  |  MAPK/ERK Pathway  |  Metabolic Enzyme/Protease

作用靶点：Amyloid-β  |  NF-κB  |  JNK  |  Endogenous Metabolite

结构分类：萜类  |  三萜

来源：植物  |  五加科  |  人参

In Vitro: Ginsenoside Re is a well-known traditional Chinese medicine, which decreases the β-site amyloid precursor protein cleaving enzyme 1 (BACE1) mRNA and protein levels and inhibits BACE1 activity in the N2a/APP695 cells. Ginsenoside Re also significantly increases the PPARγ protein and mRNA levels.To prevent Ginsenoside Re from having a cytotoxic effect on the N2a/APP695 cells, the cell viability is first determined by the MTT assay. The N2a/WT and N2a/APP695 cells are treated with increasing concentrations of Ginsenoside Re (0-200 µM) for 24 h. Ginsenoside Re concentrations under 100 µM do not affect the viability of the N2a/WT and N2a/APP695 cells, whereas the 150 µM Ginsenoside Re concentration markedly decreases the survival rate of the N2a/WT and N2a/APP695 cells. Incubation with Ginsenoside Re at a 200 µM concentration for 24 h reduces the viability of the N2a/WT and N2a/APP695 cells by 15.58% and 26.82%, respectively. These data indicate that Ginsenoside Re treatment within the range of 0-100 µM for 24 h is safe for the N2a/WT and N2a/APP695 cells (P>0.05).

In Vivo: Ginsenoside Re reduces insulin resistance in 3T3-L1 adipocytes and high-fat diet (HFD) rats through inhibition of JNK and NF-κB activation. Intraperitoneal injection of lipopolysaccharide (LPS) at a dose of 20 mg/kg is lethal to mice, and 70% to 80% of the mice die within 60 h. However, pretreatment of the mice with Rg1 or Ginsenoside Re increases their survival rates in a dose-dependent manner. With the doses of Rg1 or Ginsenoside Re increase from 2.5 to 5 mg/kg, the survival rate is elevated from 60% to 90% (Rg1) or from 30% to 40% (Ginsenoside Re). All the mice administered Rg1 at a minimal dose of 10 mg/kg are protected from death compared to 80% survival of mice treated with an equal dose of Ginsenoside Re. To protect all the mice, 20 mg/kg Ginsenoside Re is needed. To investigate the anti-inflammatory potential of Rg1 and Ginsenoside Re, 1 mg/kg Rg1 or Ginsenoside Re is injected into rats and then challenged the animals with LPS. The injection procedure itself causes a transient stress-induced increase in body temperature of ~1.2°C in each group. Thereafter, LPS-challenged rats without pretreatment develope a robust biphasic fever, with the first peak reaching ~1.5°C at 2 h and the second peak reaching 1.8°C at 4 h. In contrast, the temperature changes for the Rg1-, Ginsenoside Re-, and TAK-242-treated groups are only 0.9, 1.2, and 0.8°C at 2 h and 1.3, 1.4, and 1.0°C at 4 h, respectively. Pretreatment with Rg1, Ginsenoside Re, or TAK-242 significantly attenuates LPS-induced alterations in body temperature.

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