MicroRNA-674-5p/5-LO axis involved in autoimmune reaction of Concanavalin A-induced acute mouse liver injury.

Autoimmune hepatitis is characterized, in part, by the pathways involving cysteinyl-leukotriene metabolites of arachidonic acid, the dynamics of which remain unclear. Here, we explored post-transcriptional regulation in the 5-lipoxygenase (5-LO) pathway of arachidonic acid in a Concanavalin A (Con A) induced mouse model. We found that Con A administration lead to 5-LO overexpression and cysteinyl-leukotriene release in early hepatic injury, which was attenuated by cyclosporin A pretreatment.

Enhanced expressions and activations of leukotriene C4 synthesis enzymes in D-galactosamine/lipopolysaccharide-induced rat fulminant hepatic failure model.

Aim: To investigate the expression and activity of leukotriene C4 (LTC4) synthesis enzymes and their underlying relationship with cysteinyl leukotriene (cys-LT) generation in a rat fulminant hepatic failure (FHF) model induced by D-galactosamine/lipopolysaccharide (D-GalN/ LPS).

Methods: Rats were treated with D-GalN (300 mg/kg) plus LPS (0.1 mg/kg) for 1, 3, 6, and 12 h.

[Protective effects of triterpenoids on primarily cultured rat hepatocytes injured by D-galactosamine and carbon tetrachloride].

Objective: To investigate the protective effects and mechanism of triterpenoids on primarily cultured rat hepatocytes injured by D-galactosamine (D-GalN) or carbon tetrachloride (CCl4).

Methods: Rat hepatocytes were isolated by two-step collagenase perfusion and cultured in RPMI 1640 medium. Protective effects of asiatic acid (AA) and beta-glycyrrhetinic acid (GA) were evaluated on hepatocytes injured by D-GalN (2 mmol/L) or CCl4 (10 mmol/L).

[Gene expressions of LTC4 synthase homologs in Con A-induced mouse hepatitis and regulative effect of cyclosporine A].

Objective: To explore the gene expressions of LTC4 synthase homologs in concanavalin A (Con A)-induced mouse hepatitis and regulation role of cyclosporine A (Cs A) treatment.

Methods: Male Balb/c mouse liver injury model was developed by iv injection of Con A (20 mg/kg) and protected by Cs A pretreatment (150 mg/kg) before Con A administration. Blood samples were collected at indicated times after Con A treatment with or without Cs A pretreatment.