[Inhibition of glycogen synthase kinase 3b activity regulates Toll-like receptor 4-mediated liver inflammation].

Objective: To determine the mechanism underlying the therapeutic activities of glycogen synthase kinase 3b (GSK3b) against hepatic ischemia-reperfusion (H-IR) injury by investigating the inhibitive effects of GSK3b on inflammation mediated by Toll-like receptor 4 (TLR4).

Methods: C57BL/6 male mice were subjected to 90 min of warm liver cephalad lobe ischemia, followed by reperfusion for various lengths of time. The mice were divided into three groups: the H-IR untreated model (control group), and the H-IR inflammation-induced models that received an intraperitoneal injection of purified lipopolysaccharide (LPS) endotoxin alone (inflammation group) or with pretreatment of the SB216763 GSK3b-specific inhibitor (intervention group).

[The role of glycogen synthase kinase-3 beta in the pathogenesis of liver ischemia reperfusion injury].

Objective: To investigate the role of the key intracellular signaling molecule glycogen synthase kinase-3 beta in the mechanism of liver ischemia reperfusion (IR).

Methods: C57BL/6 mice were subjected to 90 min warm liver cephalad lobe ischemia, followed by various length of reperfusion. Experiment groups included sham control group, liver IRI model group and glycogen synthase kinase-3 beta inhibitor-treated group (SB216763 in DMSO, 25 g/kg, i.

[The approaches for making acute-on-chronic liver failure in rat].

Objective: To study the approaches for making acute-on-chronic hepatic failure model in rat.

Methods: SD rats were intraperitoneally injected with 50% CCl4 (Carbon tetrachloride) olive solution every three days for 6 or 10 weeks. Then they were divided into two groups randomly and injected with D-galactosamine (D-gal) at a dose of 2 g/kg, lipopolysaccharide (LPS) at a dose of 100 pg/kg and D-gal at a dose of 0.