Description
Neferine is a major bisbenzylisoquinline alkaloid. Neferine strongly inhibits NF-κB activation.
Solubility
DMSO : 125 mg/mL(200.07 mM;Need ultrasonic)
Source
Plants >other families
Storage
4℃, protect from light
Shipping
Room temperature in continental US; may vary elsewhere.
SMILES
OC1=CC=C(C[C@@H]2N(C)CCC3=C2C=C(OC)C(OC)=C3)C=C1OC4=CC5=C(C=C4OC)CCN(C)[C@@H]5CC6=CC=C(OC)C=C6
In Vivo
Neferine treatment at both low-dose (60 mg/kg/day by gavage) and high-dose (120 mg/kg/day by gavage) reduces the increment of collagen I, III and TGF-β1 protein expression induced by hyperglycemia.
In Vitro
Neferine down regulates hypoxia induced NF-κB p65 nuclear translocation and COX-2 expressions. Neferine reduces high-glucose-induced collagen production and inhibits TGF-β1-Smad, ERK and p38 MAPK signaling activation in cardiac fibroblasts. Cardiac fibroblasts (CFs) are cultured in HG medium with varying concentrations of Neferine (1, 2, or 5 μM). CCK-8 assays are carried out at different time points (24, 48, and 72 h). Compared with normal glucose (NG) and osmotic control (OC) treatments, High glucose (30 mM) treatment significantly increases the proliferation of CFs in a time-dependent manner (P<0.05). High glucose (HG)-induced CF proliferation is markedly attenuated by Neferine treatment at either 2 or 5 μM compared with vehicle treatment. However, 1 μM Neferine does not inhibit HG-induced proliferation of CFs. Therefore, 2 and 5 μM Neferine are used in the remaining experiments.
Datasheet 
