| Size | Price | Stock |
|---|---|---|
| 5g | $32 | In-stock |
| 10g | $50 | In-stock |
| 25g | $86 | In-stock |
| 50 g | Get quote | |
| 100 g | Get quote | |
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| Cat. No. : | HY-N0139 |
| M.Wt: | 742.68 |
| Formula: | C33H42O19 |
| Purity: | >98 % |
| Solubility: | DMSO : 100 mg/mL (ultrasonic;warming);H2O : ≥ 50 mg/mL |
Troxerutin, also known as vitamin P4, is a tri-hydroxyethylated derivative of natural bioflavonoid rutins which can inhibit the production of reactive oxygen species (ROS) and depress ER stress-mediated NOD activation. IC50 & Target: ROS[1], NOD[2] In Vitro: The results reveal that the maximum protective effect against ROS induced cell damage in the HDP cells occurs following pretreatment with 10 μM Troxerutin. Treatment with H2O2 alone decreases cell viability to 77.33±2.44%; however, pretreatment with 10 μM Troxerutin maintains cell viability at 90.88±2.24% following H2O2 exposure (P<0.05). At concentrations of 5 and 10 μM, pretreatment with Troxerutin causes a decrease in the number of cells in the sub G1 phase, indicative of cell death. In the control and Troxerutin-only-treated cells, 3.58±0.15 and 0.89±0.11% are 2′7′-dichlorofluorescein (DCF)-positive (P<0.05), whereas treatment with H2O2 alone increases the level of ROS to 46.36±2.33%. The cells pretreated with Troxerutin are 19.92±1.95% DCF-positive following H2O2 treatment, indicating that Troxerutin reduces the H2O2-induced production of ROS in the HDP cells[1] . In Vivo: Troxerutin effectively lowers body weight and obesity-related metabolic parameters in high-fat diet (HFD)-treated mice. Oral administration of Troxerutin notably inhibits those liver injuries in HFD-treated mice, restores glucose intolerance and insulin signaling, and diminishes hepatic gluconeogenesis in HFD-treated mice. Troxerutin remarkably inhibits the nuclear translocation of NF-κB p65, as well as the expressions of its target genes, in the livers of HFD-treated mice. Troxerutin also depresses endoplasmic reticulum (ER) stress-mediated Nucleotide oligomerization domain (NOD) activation in HFD-treated mouse livers[2]. Lipid depositions in tunica intimae and tunica media are attenuated in Troxerutin-treated diabetic rats compare with untreated diabetic rats. Structural disarrangement and deformity of smooth muscle cells in aortic tissue of Troxerutin-treated diabetic rats are considerably lower than histology of untreated diabetic aorta. Administration of Troxerutin for four weeks to diabetic rats significantly reduces the level of malondialdehyde (MDA) compare to that of untreated diabetic rats (P<0.01)[3].
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