Dimethyl Bisphenolate Ameliorates Carbon Tetrachloride-Induced Liver Injury by Regulating Oxidative Stress-Related Genes.

Abstract

Liver disease accounts for millions of deaths per year all over the world due to complications from cirrhosis and liver injury. In this study, a novel compound, dimethyl bisphenolate (DMB), was synthesized to investigate its role in ameliorating carbon tetrachloride (CCl4)-induced liver injury through the regulation of oxidative stress-related genes. The structure of DMB was confirmed based on its hydrogen spectrum and mass spectrometry. DMB significantly reduced the high levels of ALT, AST, DBIL, TBIL, ALP, and LDH in a dose-dependent manner in the sera of CCl4-treated rats. The protective effects of DMB on biochemical indicators were similar to those of silymarin. The ROS fluorescence intensity increased in CCl4-treated cells but significantly weakened in DMB-treated cells compared with the controls. DMB significantly increased the content of oxidative stress-related GSH, Nrf2, and GCLC dose-dependently but reduced MDA levels in CCl4-treated cells or the liver tissues of CCl4-treated rats. Moreover, DMB treatment decreased the expression levels of P53 and Bax but increased those of Bcl2. In summary, DMB demonstrated protective effects on CCl4-induced liver injury by regulating oxidative stress-related genes.