Human liver
ischemia/reperfusion injury (IRI) is a common and major clinical problem complicating liver surgery and
transplantation. The pathogenesis underlying IRI is complex, involving a series of signaling mediators and mechanisms. This study aimed to investigate the effects of
Magnesium Isoglycyrrhizinate (MgIG) on the changes of
oxidant stress and apoptosis induced by IRI in human hepatic L02 cells. L02 cells with IRI were treated with or without MgIG and
mitoKATP (Mitochondrial
adenosine triphosphate-dependent
potassium) channel modulators. Cell viability was assessed using
CCK-8 assay. Cell apoptosis was quantified by flow cytometry. The activity of the
antioxidant enzymes superoxide dismutase (SOD) and
glutathione peroxidase (GSH-Px) were measured. Effects of MgIG on the expression of Bax, Bcl-2,
Caspase 3, PARP (
poly ADP-ribose polymerase), Akt, and ERK in L02 cells with IRI were examined. Our results showed that MgIG treatment significantly reduced the population of apoptotic cells and the expression of apoptosis-related
proteins in hepatic L02 cells with IRI. MgIG also counteract
ischemia reperfusion induced oxidative challenge as it effectively reduced
malondialdehyde (MDA) and increased the activities of SOD and GSH-Px. L02 cells treated with MgIG showed increased expression of p-Akt and p-ERK, indicating that the protective effect of MgIG might be associated with the activation of Akt and ERK pathways. Moreover, the addition of
Diazoxide (DE), a
mitoKATP channel opener, enhanced the cytoprotective activity of MgIG, while the
mitoKATP blocker
5-hydroxydecanoate (5-HD) reduced the cytoprotective activity of MgIG.