Chebulic acid

Chebulic acid is a phenolic acid compound isolated from Terminalia chebula with strong antioxidant activity, which breaks protein cross-links induced by advanced glycation end products (AGEs) and inhibits the formation of AGEs. Chebulic acid is effective in controlling elevated metabolic parameters, oxidative stress, and liver damage, supporting its beneficial role in asthma, diabetes, and liver protection^{[1][2][3][4][5]}. In Vitro: Chebulic acid (0.5, 1, 5 and 10 μg/mL; 24 h) reduces UPM-induced ROS generation in NCI-H441 at doses of 5 and 10 μg/mL^[1].
Chebulic acid (5 and 10 μM; 24 h) dose-dependently reduces the expression levels of inflammatory factors in NCIH441 and dose-dependently increases the mRNA expression levels of Occludin and ZO-1 proteins in NCI-H441 in the presence of UPM^[1].
Chebulic acid (0-250 μM; 24 h) has a mild toxic effect on HUVEC at doses above 50 μM^[3].
Chebulic acid (0, 5, 10 and 25 μM; 24 h) dose-dependently reduces glycer-AGEs-induced ROS generation in HUVECs and THP-1 monocyte adhesion, and dose-dependently promotes the restoration of TER in HUVECs at doses of 10 and 25 μM^[3].
Chebulic acid (1, 10 and 100 μg/mL; 30 min) protectes hepatocytes from the cytotoxicity of t-BHP in a dose-dependent manner^[4].
Chebulic acid (0-26 μM; 24 h) increases the expression of Nrf2 in the nucleus of L-02 cells in a dose-dependent and time-dependent manner, and increases the phosphorylation levels of ERK, JNK and p38 MARK^[5].
In Vivo: Chebulic acid (37.5, 75 and 150 mg/kg; p.o.; once daily for 5 days) is non-toxic to the liver of male ICR mice, protects against CCL4-induced liver injury through Nrf2 signaling and reduces serum ALT and AST levels and liver injury levels, including reduces necrosis and histological improvement^[5].