10mM in DMSO per flussi di lavoro cromatografici e analitici sensibili che richiedono un'interferenza minima della linea di base.
Store at -80°C Spedizione Dry ice packs + Cold packs. Consultare il COA specifico del lotto per le specifiche esatte.
SDS, COA, scheda tecnica e scheda delle specifiche disponibili per il download. COA specifico del lotto accessibile tramite ricerca per numero di lotto.
Citato in 1 pubblicazioni peer-reviewed su cromatografia, sintesi organica e reazioni di accoppiamento incrociato.
Ginsenoside Rg5 is the main component of Red ginseng. Ginsenoside blocks binding of IGF-1 to its receptor with an IC 50 of ~90 nM. Ginsenoside Rg5 also inhibits the mRNA expression of COX-2 via suppression of the DNA binding activities of NF-κB p65 .
In Vitro
Ginsenoside Rg5 plays a novel role as an IGF-1R agonist. Ginsenoside Rg5 binds to IGF-1R with an IC 50 value of ~90 nM and its angiogenic activity is inhibited by IGF-1R knockdown. To investigate the possible interaction of Ginsenoside Rg5 with IGF-1R, a docking analysis is performed. Docking results show that Ginsenoside Rg5 binds strongly at two sites, A and B, with K d values of 20 and 27 nM, respectively, to the cysteine-rich domain of IGF-1R. Pretreatment with Rg5 blocks the binding of radiolabeled IGF-1 to HUVECs with an IC 50 value of ~90 μM, which is greater than an IC 50 value of ~1.4 nM for unlabeled IGF-1. The results from MTT assay show that MCF-7 cell proliferation is inhibited by Ginsenoside Rg5 treatment for 24, 48 and 72 h in a dose-dependent manner. Ginsenoside Rg5 at different concentrations (0, 25, 50 and 100 μM), induce cell cycle arrest in G0/G1 phase through regulation of cell cycle-related proteins in MCF-7 cells. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
Ginsenoside Rg5 inhibits the mRNA expression of COX-2 via suppression of the DNA binding activities of NF-κB p65 in lipopolysaccharides (LPS)-stimulated BV2 microglial cells. Rg5 pretreated group mice show declined expression of NF-κB p65 and COX-2. In the group treated with low dose of Ginsenoside Rg5 (10 mg/kg), there is remarkable tubular damage and infiltration of inflammatory cells. However, at the higher dose of Ginsenoside Rg5 (20 mg/kg), tubules markedly appeare histologically normal and no inflammation and cast formation is observed in kidney tissues. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal administration
Mice Male ICR mice (6 to 8 weeks old), weighing 25-27 g , are used. After acclimation for one week, mice are randomly assigned into 4 experimental groups with 8 mice in each group: normal control, Cisplatin control, and Cisplatin+ Ginsenoside Rg5 groups (10 and 20 mg/kg, respectively) . Ginsenoside Rg5 is administered intragastrically at the dose of 10 and 20 mg/kg for 10 days. On the 7th day, animals in Cisplatin control and Ginsenoside Rg5-treated groups receive a single intraperitoneal injection of Cisplatin (25 mg/kg) to induce nephrotoxicity in mice. Mice are anaesthetized with pentobarbital, subsequently sacrificed at 72 h after Cisplatin injection (Day 10). Blood samples are collected and then centrifuged at 3000 rpm to separate the serum and stored at -20 °C for determining blood urea nitrogen (BUN) and creatinine (CRE) levels. aladdin has not independently confirmed the accuracy of these methods. They are for reference only.
IC50& Target:IGF-1R|90 nM (IC|50|)|p65|COX-2
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