Background and Aims:Reactive oxygen species (ROS) are considered to play a prominent causative role in the development of various hepatic disorders. Antioxidants have been demonstrated effectively to protect against hepatic damage. Hydrogen (H2), a new antioxidant, was reported to selectively reduce the strongest oxidants, such as hydroxyl radicals (·OH) and peroxynitrite (ONOO-), and did not disturb metabolic oxidation-reduction reactions or disrupt ROS involved in cell signaling. In contrast to H2 gas, hydrogen-rich saline (HS) may be more suitable for clinical application. We here aim to verify its protective effects in experimental models of liver injury.Methods:H2 concentration in vivo was detected by hydrogen microelectrode for the first time. Liver damage, ROS accumulation, cytokine levels and apoptotic protein expression were evaluated after GaIN/LPS, CCl4 and DEN challenge, respectively. Simultaneously, CCl4-induced hepatic fibrosis and DEN-induced hepatocyte proliferation were measured.Results:HS predominantly increased hydrogen concentration in liver and kidney tissue. Actue liver injury, hepatic fibrosis and hepatocyte proliferation were reduced by quenching exclusively detrimental ROS. Pro-apoptotic players such as JNK and caspase-3 activity were inhibited.Conclusions:HS could not only apparently protect against the liver injury but also inhibite the process of liver fibrosis and hepatocyte compensatory proliferation.
|