Women aged 50 - 80 years were given two cookies enriched with 9.2 mg avenanthramide (per two cookies) daily for 8 weeks. Before and after consuming the cookies the women walked downhill on a treadmill for 4 bouts of 15 min. Blood samples were collected before and after supplementation at rest and 24 post walking, and 48 hours post walking. Chronis supplementation was observed to decrease inflammation and increased blood-borne antioxidant defense in menopausal women.

Adherent primary osteoblastic C57BL/6 wild-type and Nrf2 knock-out (KO) cells were cultured in a medium of alpha-Minimum Essential Medium Eagle (MEM) with 10% fetal bovine serum (FBS), 1% penicillin/streptomycin, and 50 mg/mL normocin. Adherent OB-6 osteoblastic cells were grown in alpha-MEM with 10% FBS, and 1% penicillin/streptomycin and 50 mg/mL normocin. Non-adherent cells were grown in alpha-MEM with 10% FBS and 1% penicillin/streptomycin, and 80 ng/mL of recombinant murine soluble Receptor Activator for Nuclear Factor κB Ligand (sRANKL) and 20 ng/mL recombinant murine Macrophage Colony Stimulating Factor (M-CSF). Cells were treated for 24 hours with 1 microM Avenathramide 2p. Mature osteoclasts were examined for viability and activity of the osteoclast-specific enzyme TRAPase using a commercial TRAPase staining kit. Avenanthramide 2p (AVA-2p) increased COL1A expression in OB-6 cells. In MLO-Y4 cells, AVA-2p increased the expression of RANKL. Even at low doses, AVA-2p blocks the etoposide-induced apoptosis of osteoblastic cells, and one hour of pre-treatment prevents dexamethasone or H2O2 induced OB-6 and MLO-Y4 cell death.