1,3-Dicaffeoylquinic acid (Synonyms: 1,5-DCQA, 1,3-Dicaffeoylquinic Acid)

1,3-Dicaffeoylquinic acid is a caffeoylquinic acid derivative that exhibits antioxidant activity and radical scavenging activity. Akt PI3K

1,3-Dicaffeoylquinic acid shows increased neuronal cell viability against Aβ(42) toxicity in a concentration-dependent manner in neurons. 1,3-Dicaffeoylquinic acid activates both phosphoinositide 3-kinase (PI3K)/Akt and extracellular regulated protein kinase 1/2 (Erk1/2) with stimulating their upstream tyrosine kinase A (Trk A). 1,3-Dicaffeoylquinic acid's anti-apoptotic potential is related to the enhanced inactivating phosphorylation of glycogen synthase kinase 3β (GSK3β) and the modulation of expression of apoptosis-related protein Bcl-2/Bax[2]. 1,3-Dicaffeoylquinic acid (10 μM, 20 μM, 50 μM, and 100 μM) significantly increases cell viablity before OGD/reperfusion, and prevents the depletion of GSH under OGD/reperfusion insult. 1,3-Dicaffeoylquinic acid induces nuclear translocation of Nrf2 in OGD/reperfusion treated astrocytes, and induces increased GCL activity, and the effect is lost in Nrf2 siRNA-transfected cells[3].

1,3-Dicaffeoylquinic acid (32.0 mg/kg, p.o.) and 1-O-ABL are absorbed very quickly in Wistar rats. The maximum plasma concentrations for 1,3-Dicaffeoylquinic acid and 1-O-ABL are 44.5 ± 7.1 and 19.1 ± 6.9 ng/mL, respectively[1].

[1]. Wang Z, et al. An LC-MS/MS method for simultaneous determination of 1,5-dicaffeoylquinic acid and 1-O-acetylbritannilactone in rat plasma and its application to a pharmacokinetic study. [2]. Xiao HB, et al. 1,5-dicaffeoylquinic acid protects primary neurons from amyloid β 1-42-induced apoptosis via PI3K/Akt signaling pathway. Chin Med J (Engl). 2011 Sep;124(17):2628-35. [3]. Cao X, et al. 1, 5-Dicaffeoylquinic acid-mediated glutathione synthesis through activation of Nrf2 protects against OGD/reperfusion-induced oxidative stress in astrocytes. Brain Res. 2010 Aug 6;1347:142-8.