Deacetylasperulosidic Acid

Deacetylasperulosidic Acid is an orally active antioxidant. Deacetylasperulosidic Acid exerts a definite in vivo antioxidant effect and alleviates oxidative stress injury by enhancing SOD activity. In atopic dermatitis models, Deacetylasperulosidic Acid corrects Th2-skewed immune imbalance and reduces allergy-related factors; in immunosuppression models, it activates cellular immunity, enhances NK cell activity and IL-2 production. Deacetylasperulosidic Acid can be used in the research of atopic dermatitis^[1][2][3]. In Vitro:Deacetylasperulosidic Acid reduced 4-nitroquinoline 1-oxide-induced genotoxicity by 98.96%^[1].
Deacetylasperulosidic Acid inhibited low-density lipoprotein oxidation^[1].
Deacetylasperulosidic Acid inhibited release of tumor necrosis factor-alpha^[1].
Deacetylasperulosidic Acid suppressed the induction of chromosome aberrations^[1].
Deacetylasperulosidic Acid demonstrates anti-atopic activity in human HaCaT keratinocytes, HMC-1 mast cells, and EOL-1 eosinophils by supporting immune balance and skin barrier function^[3]. In Vivo:Deacetylasperulosidic Acid (15-60 mg/kg; p.o.; daily; 7 days) exerts dose-dependent in vivo antioxidant activity in Wistar rats, with significant reductions in serum MDA (19.7-22.6%) and increases in serum SOD activity (11.3-13.0%) at doses of 30 and 60 mg/kg body weight administered daily for 7 days^[1].
Deacetylasperulosidic Acid (30-100 mg/kg; p.o.; daily; 14 days) at 100 mg/kg inhibits EC₅₀-induced reduction of IL-2 production, while 30 mg/kg and 100 mg/kg increase NK cell cytotoxicity to 12% and 21%, respectively, with no impact on splenic lymphocyte subpopulations^[2].
Deacetylasperulosidic acid (3-12 mg/kg; p.o.; daily; 4 weeks) alleviates atopic dermatitis in DNCB-induced NC/Nga mice in a dose-dependent manner by reducing pruritus, restoring immune balance, and repairing skin barrier function, with the 12 mg/kg dose achieving near-normal levels for most measured parameters^[3].