Statin induces apoptosis of human colon cancer cells and downregulation of insulin-like growth factor 1 receptor via proapoptotic ERK activation.

Insulin-like growth factor 1 (IGF-1) and IGF-1 receptor (IGF-1R) signaling plays an important role in tumor progression in patients with certain gastrointestinal tract cancers. In addition to lowering cholesterol in serum, statins have pleiotropic effects, including anti-oxidative, anti-inflammatory or anti-neoplastic effects. Therefore, the present study investigated whether statins could induce the apoptosis of colon cancer cells and regulate the expression of IGF-1R and its associated signaling pathways in the present study.

Upper gastrointestinal bleeding in severely burned patients: a case-control study to assess risk factors, causes, and outcome.

Background/aims: To determine the risk factors, causes, and outcome of clinically important upper gastrointestinal bleeding that occurs in severely burned patients.

Methodology: The charts of all patients admitted to the burn intensive care unit were analyzed retrospectively over a 4-year period (from January 2006 to December 2009). Cases consisted of burned patients who developed upper gastrointestinal bleeding more than 24 hours after admission to the burn intensive care unit.

Pravastatin activates the expression of farnesoid X receptor and liver X receptor alpha in Hep3B cells.

Background: Statins are suggested to preserve gallbladder function by suppressing pro-inflammatory cytokines and preventing cholesterol accumulation in gallbladder epithelial cells. They also affect cross-talk among the nuclear hormone receptors that regulate cholesterol-bile acid metabolism in the nuclei of hepatocytes. However, there is controversy over whether or how statins change the expression of peroxisome proliferator-activated receptor (PPAR)alpha, PPARgamma, liver X receptor alpha (LXRalpha), farnesoid X receptor (FXR), ABCG5, ABCG8, and 7alpha-hydroxylase (CYP7A1) which are directly involved in the cholesterol saturation index in bile.

The effect of PPARalpha and PPARgamma ligands on inflammation and ABCA1 expression in cultured gallbladder epithelial cells.

The preservation of gallbladder function by control of inflammation and elimination of cholesterol accumulation in gallbladder epithelial cells (GBEC) could contribute to the prevention of gallstone formation and cholecystitis. Peroxisome proliferator-activated receptors (PPARs) modulate inflammation and lipid metabolism in various cells and GBEC efflux of excessive amounts of absorbed cholesterol through the ATP-binding cassette transporter A1 (ABCA1)-mediated pathway. The aim of this study was to determine whether ligands of PPARalpha and PPARgamma modulate inflammation and have an effect on ABCA1 expression in GBEC.