Description |
Nothofagin, a dihydrochalcone, is isolated from rooibos (Aspalathus linearis)[1]. Nothofagin downregulates NF-κB translocation through blocking calcium influx. Nothofagin has antioxidant activity and ameliorates various inflammatory responses such as the septic response and vascular inflammation[2].
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In Vitro |
Nothofagin pre-treatment (0.1, 1, 10 μM) decreases the level of histamine release in RBL-2H3 and RPMCs cells. The production of cytokines are downregulated bynothofagin pre-treatment Nothofagin (TNF-α: 1-10 μM; IL-4: 0.1-10 μM, IL-6: 1-10 μM)[1]. Pre-treatment of DNPHSA-stimulated RBL-2H3 with Nothofagin (10 μM) markedly suppresses the phosphorylation of Lyn, Syk, and Akt[1]. Nothofagin (30 μM; for 6 hours) results in inhibited formation of LPS-induced (100 ng/mL; 4 hours) paracellular gaps with the formation of dense F-actin rings in HUVECs[2]. Nothofagin suppresses IgE-mediated mast cell degranulation both in vitro and in vivo[1].
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In Vivo |
Nothofagin (1 mg/kg; orally; once a day; for 7 days) significantly increases the urinary volume of both normotensive (NTR) and spontaneously hypertensive rats (SHR)[3]. Animal Model: Male Wistar normotensive and spontaneously hypertensive rats (3-4 months old) [3] Dosage: 1 mg/kg Administration: Orally; once a day; for 7 days Result: Significantly increased the urinary volume of both NTR and SHR.
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Density | 1.594±0.06 g/cm3 |
Boiling Point | 711.5±0.0 °C at 760 mmHg |
Flash Point | 249.4±0.0 °C |
Exact Mass | 436.136932 |
LogP | 0.90 |
Vapour Pressure | 0.0±0.0 mmHg at 25°C |