Pterostilbene induces cell cycle arrest and apoptosis in MOLT4 human leukemia cells.

Pterostilbene, a polyphenolic compound present in grapes and other fruits, has been demonstrated to inhibit growth and induce apoptosis and autophagy in some cancer cell types. We found that pterostilbene at the IC(90) concentration of 44 µM inhibited proliferation and induced apoptosis in MOLT4 human leukemia cells. Treatment with pterostilbene resulted in a transient accumulation of cells in the G(0)/G(1)-cell cycle phase followed by the S-phase arrest.

Feedback inhibition of cholesterol biosynthesis by dietary cholesterol in experimental chronic renal failure.

Objective: Enhanced liver cholesterol synthesis is present in experimental chronic renal failure (CRF), even though cholesterol concentrations in blood and liver are increased, suggesting that CRF results in disturbed cholesterolegenesis feedback regulation.

Design: This study sought to elucidate whether dietary cholesterol exerts inhibitory effects on liver cholesterologenesis in CRF rats.

Methods: Male Wistar rats were used.

Increased gene expression of liver SREBP-2 in experimental chronic renal failure.

Sterol regulatory element-binding protein-2 (SREBP-2) is a transcription factor regarded as the main regulator of cholesterol homeostasis. Therefore, increased level of SREBP-2 could be responsible for hypercholesterolemia, which is observed in experimental chronic renal failure (CRF). This study was designed primary to evaluate the impact of experimental CRF (5/6 nephrectomy model) on rat liver SREBP-2 gene expression.

Does resveratrol prevent free radical-induced acute pancreatitis?

Objective: The purpose of this study was to examine protective and antioxidative effect of stilbene derivatives, resveratrol and diethylstilbestrol, in experimental acute pancreatitis (EAP).

Methods: EAP was induced in male Wistar rats by retrograde injection of tert-butyl hydroperoxide (ButOOH) solution, a well-known prooxidant agent, into the common bile pancreatic duct. After a 3-hour observation, the animals were killed.

[Pathomechanism of hyperlipoproteinemia in chronic renal failure].

Lipid disorders are one of the known metabolic changes associated with chronic renal failure (CRF) [1, 2]. They are present as: hypertriglyceridemia--existed in 60% of CRF patients and hypercholesterolemia observed in 20-30% of people with this syndrome. These disorders, what was shown also in our own studies, are existing in different intensity in patients treated with maintenance haemodialysis [3], peritoneal dialysis [4] and after renal transplantation as well [5].

Contribution of increased HMG-CoA reductase gene expression to hypercholesterolemia in experimental chronic renal failure.

The aim of the present study was to examine hypothesis that the enhanced cholesterologenesis, found in rats with experimental chronic renal failure (CRF) resulted from the increased gene expression of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase--the rate limiting enzyme in the cholesterologenesis pathway, responsible for mevalonate synthesis. Wistar rats were used and experimental CRF was achieved by 5/6 nephrectomy model. We examined: (a) the changes in the rat liver microsomal HMG-CoA reductase activity, (b) the rat liver HMG-CoA reductase mRNA abundance in various times of day.