High concentration of magnolol induces hepatotoxicity under serum-reduced conditions.

Although magnolol is cytoprotective against warm ischemia/reperfusion injury, its effect on cold preservation has not been fully investigated. This study aimed at examining whether magnolol maintains the liver graft integrity after cold preservation and elucidating the underlying mechanisms in terms of apoptotic signaling under both normothermic and hypothermic conditions. After being preserved in Ringer's lactate (RL) at 4 degrees C for 6h ex vivo, the magnolol-treated grafts demonstrated significantly higher AST, ALT, and LDH levels in perfusates than those from negative controls.

Serum factors potentiate hypoxia-induced hepatotoxicity in vitro through increasing transforming growth factor-beta1 activation and release.

Background: Although transforming growth factor-beta (TGF-beta), a growth regulator of hepatocytes, induces cell death under pathological conditions, responsiveness of hepatocytes to hypoxic stimulus has not been fully defined. This study aimed at investigating the role of TGF-beta1 in hypoxia-induced hepatotoxicity using cultured clone-9 hepatocytes with or without serum supplementation.

Methods/results: Presence of serum significantly potentiated hypoxia-induced hepatotoxicity after 72h of exposure, as evidenced by fluorescent viability stain and LDH cytotoxicity assay.

Propofol pretreatment attenuates LPS-induced granulocyte-macrophage colony-stimulating factor production in cultured hepatocytes by suppressing MAPK/ERK activity and NF-kappaB translocation.

Propofol (PPF), a widely used intravenous anesthetic for induction and maintenance of anesthesia during surgeries, was found to possess suppressive effect on host immunity. This study aimed at investigating whether PPF plays a modulatory role in the lipopolysaccharide (LPS)-induced inflammatory cytokine expression in a cell line of rat hepatocytes. Morphological observation and viability assay showed that PPF exhibits no cytotoxicity at concentrations up to 300 microM after 48 h incubation.

Heat preconditioning ameliorates hepatocyte viability after cold preservation and rewarming, and modulates its immunoactivity.

Background: Heat preconditioning significantly preserved liver graft function after cold preservation in animal experimental model. The elevation of heat shock protein 70 (HSP70) was claimed to play a critical role in protecting grafts against cold preservation-induced hepatocyte apoptosis. However, little is known about whether HSP70 also plays an immunomodulatory role in cold preserved cells.