Nothofagin

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]. 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].
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].