Rosmarinic acid Ameliorates H2O2-Induced Oxidative Stress On L02 Cells through MAPK and Nrf2 Pathways.

Liver cells are easy to be damaged by oxidative stress during the progression both liver development and throughout adult life, resulting in tissue pathology which ranges from simple hepatitis to non-alcoholic fatty liver disease (NAFLD). Here, we determined the attenuation of oxidative stress on liver cells with pre-treatment of Rosmarinic acid (RA), which is an antioxidant agent from Rosmarinus officinalis. Human liver cell line L02 was damaged by hydrogen peroxide (H2O2). In the RA treatment group, the viability of L02 cells increased and the intracellular reactive oxygen species (ROS) levels decreased compared with the H2O2-induced damage group. Analysis of the flow cytometry revealed that the percentage of G2/M cell cycle arrest and cell apoptosis decreased in the RA treatment group. This alteration was associated with activation of a G2/M DNA damage and oxidative stress apoptotic signal. Furthermore, we determined the redox-sensitive protein expression of mitogen-activated protein kinases (MAPKs), quinone acceptor oxidoreductase 1 (NQO1) and nuclear factor E2-related factor 2 (Nrf2), and the expression of MAPKs and Nrf2 were both activated in the RA group. Results showed that the relevant protein expression of MAPKs and Nrf2 were activated in the RA group. Thus, RA protected L02 cells from oxidative damage through suppre.