A comparison of blood and cerebrospinal fluid cytokines (IL-1β, IL-6, IL-18, TNF-α) in neonates with perinatal hypoxia.

Perinatal hypoxia-ischemia is a specific and important pathological event in neonatal care practice. The data on relationship between the concentrations of cytokines in blood and cerebrospinal fluid (CSF) and perinatal brain injury are scarce. The aim of this study is to evaluate changes in interleukin (IL-1β, IL-6, and IL-18) and tumor necrosis factor alpha (TNF-α) levels in newborns with perinatal hypoxia (PNH).

Anti-Inflammatory Effects of Hyperbaric Oxygenation during DSS-Induced Colitis in BALB/c Mice Include Changes in Gene Expression of , Proinflammatory Cytokines, and Antioxidative Enzymes.

Reactive oxygen species (ROS) and nitrogen species have an indispensable role in regulating cell signalling pathways, including transcriptional control via hypoxia inducible factor-1 (). Hyperbaric oxygenation treatment (HBO) increases tissue oxygen content and leads to enhanced ROS production. In the present study DSS-induced colitis has been employed in BALB/c mice as an experimental model of gut mucosa inflammation to investigate the effects of HBO on , antioxidative enzyme, and proinflammatory cytokine genes during the colonic inflammation.

The effect of glucagon and cyclic adenosine monophosphate on acute liver damage induced by acetaminophen.

Recent investigations suggest that glucagon might have a potentially important hepatoprotective activity. We investigated the effect of glucagon in a model of acetaminophen-induced liver injury. CBA male mice were injected intraperitoneally with a lethal (300 mg/kg) or sublethal (150 mg/kg) dose of acetaminophen.

The role of prostaglandin E2 in acute acetaminophen hepatotoxicity in mice.

Prostaglandin E2 (PGE2), which is synthesized by many cell types, has a cytoprotective effect in the gastrointestinal tract and in several other tissues and cells. On the other hand, overdose or chronic use of a high dose of acetaminophen (Paracetamol, APAP) is a major cause of acute liver failure in the western world. These observations prompted us to investigate whether PGE2 plays a role in host defence to toxic effect of APAP.