Avenanthramide C

Avenanthramide C is an orally active polyphenolic compound that penetrates the blood-brain barrier. Avenanthramide C is derived from oats. Avenanthramide C inhibits NF-κB nuclear translocation and inhibits the phosphorylation of PI3K, PLCγ1, Lyn, Syk, and Akt. Avenanthramide C inhibits the expression and activity of MMP-9 and inhibits MAPK phosphorylation. Avenanthramide C scavenges DPPH radicals, reduces intracellular ROS, and inhibits pro-inflammatory cytokine release and adhesion molecule expression. Avenanthramide C inhibits cell degranulation. Avenanthramide C attenuates active systemic anaphylaxis and inhibits passive cutaneous anaphylaxis. Avenanthramide C ameliorates PHZ-induced blood stasis. Avenanthramide C inhibits neuroinflammation, restores long-term potentiation, and improves recognition and spatial memory in Alzheimer's disease models. Avenanthramide C can be used for research on allergic inflammation, thrombosis, atherosclerosis, and Alzheimer's disease^{[1][2][3][4][5]}. In Vitro:Avenanthramide C (0.01-100 µM; 12 h) is not cytotoxic up to 100 µM in RBL-2H3 cells^[1].
Avenanthramide C (1-100 nM; 1 h) concentration-dependently inhibits β-hexosaminidase release in DNP-HSA-stimulated RBL-2H3 cells^[1].
Avenanthramide C (1-100 nM; 1 h) concentration-dependently inhibits histamine release in DNP-HSA-stimulated RBL-2H3 cells^[1].
Avenanthramide C (1-100 nM) suppresses DNP-HSA-stimulated intracellular calcium elevation in a concentration-dependent manner in RBL-2H3 cells^[1].
Avenanthramide C (1-100 nM; 1 h) inhibits DNP-HSA-stimulated phosphorylation of PI3K and PLCγ1 in RBL-2H3 cells^[1].
Avenanthramide C (1-100 nM; 1 h) concentration-dependently inhibits the gene expression and release of IL-4, IL-6, and TNF-α in DNP-HSA-stimulated RBL-2H3 cells^[1].
Avenanthramide C (1-100 nM; 1 h) inhibits the phosphorylation of Lyn, Syk, and Akt and suppresses IκBα degradation and NF-κB nuclear translocation in DNP-HSA-stimulated RBL-2H3 cells^[1].
Avenanthramide C (0-100 μM; 24 h) dose-dependently suppresses the TNF-α-induced increase in MMP-9 mRNA levels in HASMC cells^[3].
Avenanthramide C (100 μM) inhibits the MAPK signaling pathway by decreasing phosphorylation of ERK, JNK, and p38, and reduces IκB phosphorylation in TNF-α-stimulated HASMC cells^[3].
Avenanthramide C (50 μM; 2 h) restores impaired LTP in ex vivo hippocampal slices from 5XFAD mice^[5].
Avenanthramide C (50 μM; 2 h) restores impaired LTP in ex vivo hippocampal slices from Tg2576 mice^[5].
Avenanthramide C (1.0625-100 μg mL^-1; 30 min) acts as a potent free radical scavenger in the cell-free DPPH assay with an IC₅₀ of 7.38 μg mL^-1[2].
Avenanthramide C (6.25-100 μg mL^-1; 24 h) is non-toxic to HUVECs at concentrations up to 25 μg mL^-1 but exhibits cytotoxic effects at 50 and 100 μg mL^-1[2].
Avenanthramide C (6.25-25 μg mL^-1; 24 h) dose-dependently attenuates intracellular ROS accumulation induced by t-BOOH in HUVECs^[2]. In Vivo:Avenanthramide C (0.1-10 mg/kg; p.o.; administered on days 9, 11, and 13) dose-dependently attenuates ovalbumin-induced active systemic anaphylaxis by suppressing the decrease in body temperature and reducing elevated serum histamine, IgE, and IL-4 levels^[1].
Avenanthramide C (0.1-10 mg/kg; p.o.; single dose; 1 h before DNP-HSA challenge) dose-dependently inhibits IgE-mediated passive cutaneous anaphylaxis^[1].
Avenanthramide C (6 mg/kg; p.o.; daily; 2 weeks) rescues impaired long-term potentiation in 5XFAD Alzheimer's disease model mice^[5].
Avenanthramide C (6 mg/kg; p.o.; daily; 2 weeks) rescues impaired long-term potentiation in Tg2576 Alzheimer's disease model mice^[5].
Avenanthramide C (6 mg/kg; p.o.; once daily; 2 weeks) inhibits neuroinflammation in the hippocampus of 5XFAD and Tg2576 Alzheimer's disease model mice^[5].