Lipid accumulation in concanavalin A-induced hepatitis: Another cause for impaired liver regeneration afterwards?

Derangements of liver tissue bioenergetics in Concanavalin A-induced hepatitis

BACKGROUND A novel in vitro system was employed to investigate liver tissue respiration (mitochondrial O2 consumption) in mice treated with concanavalin A (Con A). This study aimed to investigate hepatocyte bioenergetics in this well-studied hepatitis model. METHODS C57Bl/6 and C57Bl/6 IFN-γ-/- mice were injected intravenously with 12 mg ConA/kg. Liver specimens were collected at various time...

Protective effect of interleukin-36 receptor antagonist on liver injury induced by concanavalin A in mice

Objective(s): Interleukin-36 receptor antagonist (IL-36Ra) is a new member of the IL-1 family that exhibits anti-inflammatory activity in a variety of inflammatory and immune diseases. Our purpose was to determine the effect of IL-36Ra on liver injury in a mouse hepatitis model induced by concanavalin A (ConA). Materials and Methods: Mic...

Hepatitis the Liver in Concanavalin A-Induced Essential Role for Neutrophil Recruitment to

NKT Cells + Accumulation and Activation of Liver CD4 A-Induced Hepatitis via Promoting TLR-9 Activation Aggravates Concanavalin

Concanavalin-A-induced liver injury is severely impaired in mice deficient in P-selectin.

P-selectin (CD62P) is an adhesion molecule that mediates the initial attachment of leukocytes to activated platelets and endothelial cells in damaged tissues. We evaluated the role of P-selectin in concanavalin A (Con A)-induced hepatitis, a model characterized by CD4(+) T cell activation and infiltration of the liver. Con A injection induced transient P-selectin expression on hepatic venules a...