Chicoric acid (Synonyms: L-Chicoric Acid, Dicaffeoyltartaric Acid, NSC 99173)

Chicoric acid (Cichoric acid), an orally active dicaffeyltartaric acid, induces reactive oxygen species (ROS) generation. Chicoric acid inhibits cell viability and induces mitochondria-dependent apoptosis in 3T3-L1 preadipocytes through ROS-mediated PI3K/Akt and MAPK signaling pathways. Chicoric acid increases glucose uptake, improves insulin resistance, and attenuates glucosamine-induced inflammation. Chicoric acid has antidiabetic properties and antioxidant, anti-inflammatory effects[1][2][3].

Chicoric acid (Cichoric acid; 10-200 μM; for 24, 48, and 72 h) causes a dose- and time-dependent decrease in cell viability[1]. Chicoric acid (100 μM; 48 h) induces apoptosis through caspase-3-dependent pathway[1]. Chicoric acid (100 μM; 48 h) decreases the protein level of p-Akt[1]. Chicoric acid (25, 50, 100 µM; for 24 hours) dramatically improves glucose uptake in a dose-dependent manner, and Chicoric acid further enhances insulin-induced (100 nM; 30 min) glucose uptake by 57.7% in HepG2 cells[2]. Chicoric acid (100 µM; for 24 hours) restores glucosamine-induced impairment of GLUT2 translocation through activating PI3K/Akt pathway in HepG2 cells[2]. Chicoric acid (100 µM) has no effects on HepG2 cell viability[2].

Chicoric acid (Cichoric acid; 60 mg/kg/day; drinking water for 4 weeks) inhibits pancreas apoptosis and adjusts islet function in diabetic mice, leading to an increase in insulin generation and secretion in C57BL/6J mice with Streptozotocin (STZ; 50 mg/kg; ip; for consecutive 5 days)[3].

[1]. Haifang Xiao, et al. Chicoric acid induces apoptosis in 3T3-L1 preadipocytes through ROS-mediated PI3K/Akt and MAPK signaling pathways. J Agric Food Chem. 2013 Feb 20;61(7):1509-20.
[2]. Di Zhu, et al. Cichoric Acid Reverses Insulin Resistance and Suppresses Inflammatory Responses in the Glucosamine-Induced HepG2 Cells. J Agric Food Chem. 2015 Dec 30;63(51):10903-13.
[3]. Di Zhu, et al. Cichoric acid improved hyperglycaemia and restored muscle injury via activating antioxidant response in MLD-STZ-induced diabetic mice. Food Chem Toxicol. 2017 Sep;107(Pt A):138-149.