Effects of urotensin-II on cytokines in early acute liver failure in mice.

Aim: To investigate urotensin-II (UII) and its effects on tumor necrosis factor (TNF)-α and interleukin (IL)-1β in early acute liver failure (ALF).

Methods: We investigated the time-dependent alteration in UII levels and its effects on TNF-α and IL-1β in liver and blood in the early stage of lipopolysaccharide/D-galactosamine-induced ALF.

Results: After lipopolysaccharide/D-galactosamine challenge, UII rose very rapidly and reached a maximal level 0.

The UII/UT system mediates upregulation of proinflammatory cytokines through p38 MAPK and NF-κB pathways in LPS-stimulated Kupffer cells.

The urotensin II (UII)/UII receptor (UT) system is closely related to immune inflammation. In acute liver failure (ALF), the UII/UT system can promote the production and release of proinflammatory cytokines, inducing an inflammatory injury response in liver tissue. However, the mechanism by which the hepatic UII/UT system promotes proinflammatory cytokine production and release is not clear.

Inhibition of UII/UTR system relieves acute inflammation of liver through preventing activation of NF-κB pathway in ALF mice.

Urotensin II (UII) is implicated in immune inflammatory diseases through its specific high-affinity UT receptor (UTR). Enhanced expression of UII/UTR was recently demonstrated in the liver with acute liver failure (ALF). Here, we analysed the relationship between UII/UTR expression and ALF in lipopolysaccharide (LPS)/D-galactosamine (GalN)-challenged mice.

[Inhibitive mechanisms of Pim-3 affecting fulminant hepatic apoptosis].

To investigate the mechanisms of serine/threonine kinase Pim-3 inhibition of fulminant hepatic apoptosis. Thirty-two rats were randomly divided into four groups (n = 8 each): normal controls (A); pretreatment with Ringer's solution (B), vector plasmid (C), or Pim-3 recombinant plasmid (D) by hydrodynamics-based procedure followed by intraperitoneal injections of lipopolysaccharide (LPS) and D-galactosamine (D-GalN) after one day. At 8 h after the LPS/D-GalN injections, liver tissues were collected from all groups of mice and analyzed for cell apoptosis by detecting caspase-3 activity (measured in relative fluorescence units, RFU).

[Effects of urantide, a urotensin receptor inhibitor, on acute hepatocyte apoptosis in mice].

Objective: To explore the effects of urantide, a urotensin II receptor (UT) inhibitor, on lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced acute hepatocyte apoptosis in mice.

Methods: Male BALB/c mice were randomly divided into 4 groups (n = 6 each): normal control, pre-treatment control, model and pre-treatment model. The pre-treatment control and pre-treatment model groups received urantide (0.