Vitamin D protects against prednisolone-induced liver injury associated with the impairment of the hepatic NF-κB/iNOS/NO pathway.

The study was carried out to define whether prednisolone-induced damage to hepatic cells is accompanied by excessive nitric oxide (NO) levels associated with nuclear factor kappa B (NF-κB)/inducible NO synthase (iNOS) activation and evaluate the efficacy of the treatment with vitamin D. Histopathological examination, activities of liver transaminases (alanine aminotransferase and aspartate aminotransferase), and cell death assays consistently showed that prednisolone (5 mg/kg body weight, 30 days) induces chronic liver injury in female Wistar rats. Specifically, increased hepatocellular necrosis and caspase-3-dependent apoptosis were observed.

Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells.

The study was designed to evaluate reactive oxygen species (ROS)/nitric oxide (NO) formation and apoptotic/necrotic cell death elicited by prednisolone in peripheral blood and bone marrow mononuclear cells and to define the efficacy of vitamin D3 to counter glucocorticoid (GC)-induced changes. It was shown that prednisolone (5 mg per kg of female Wistar rat’s body weight for 30 days) evoked ROS and NO overproduction by blood mononuclear cells (monocytes and lymphocytes) that correlated with increased cell apoptosis and necrosis. In contrast, prednisolone did not affect ROS/NO levels in bone marrow mononuclear cells that corresponded to lower level of cell death than in the control.

Role of vitamin D3 in regulation of interleukin-6 and osteopontin expression in liver of diabetic mice.

Objective: To study the link between hepatic interleukin-6 (IL-6) and osteopontin (OPN) gene expression and vitamin D3 status associated with type 1 diabetes in mice; and to evaluate the effects of vitamin D3 treatment (800 IU/kg of body weight for 6 weeks) on diabetes-induced impairments.

Materials And Methods: mRNA levels of IL-6 and OPN were measured by quantitative RT-PCR. Blood serum 25OHD3 was assayed by ELISA.

[Not Available].

The mechanisms of diabetes-associated impairment of cellular immune defense and its regulation by vitamin D3 are not fully elucidated. The study was devoted to investigating the functional state of T-cell immunity as well as humoral immune activity in response to artificial immunization in experimental diabetes and after prolonged administration of vitamin D3. It was established that diabetes is characterized by a 2.

Effects of vitamin D3 and vitamin E on prednisolone-induced alterations of phagocyte function.

Objective: To evaluate the effectiveness of vitamin D3 and its combined action with vitamin E in the correction of the impairments of phagocyte function caused by chronic glucocorticoid administration.

Materials And Methods: Phagocytic activity was assessed by the ability of peripheral blood neutrophils and monocytes to capture FITC-labeled Escherichia coli using flow cytometry. Metabolic activity of neutrophils was measured cytochemically as nitro blue tetrazolium (NBT) reduction test.

[The role of vitamin D3 in the regulation of the mineral metabolism in experimental type 1 diabetes].

Diabetes was shown to be associated with a considerable lowering of 25(OH)D3 in blood serum of mice. Vitamin D3 deficiency was correlated with impaired mineral metabolism in bone tissue, indicating the development of secondary osteoporosis. A decrease in weight, length and diameter (diaphysis, proximal metaepiphysis) of tibia in diabetic animals was observed as compared with control.

1-methylnicotinamide (MNA) in prevention of diabetes-associated brain disorders.

The present study has been designed to establish the potential benefits from 1-methylnicotinamide (MNA) treatment on brain disorders associated with type 1 diabetes. All experiments were carried out after 6 weeks of streptozotocin-induced diabetes (60 mg/kg of body weight, i.p.

Effects of nicotinamide supplementation on liver and serum contents of amino acids in diabetic rats.

Objective: Diabetes-related metabolic impairments may be associated with altered protein and amino acid turnover. The goal of the current research was to estimate possible changes in amino acid profiles in rat serum and liver. We also studied whether nicotinamide (NAm), as a drug with the wide range of metabolic effects, can influence metabolic impairments associated with diabetes.

Poly(ADP-ribosyl)ation enhancement in brain cell nuclei is associated with diabetic neuropathy.

Unlabelled: The study has been undertaken to evaluate the effect of streptozotocin (STZ)-induced diabetes on rat brain poly(ADP-ribose)polymerase (Parp) activity and assess whether and how a Parp inhibitor, nicotinamide (NAm), may potentially regulate the diabetes-induced changes. Experiments were carried out after 4 weeks of diabetes duration in rats treated with or without NAm (100 or 200 mg kg(-1) day(-1), injected intraperitonally for 2 weeks). Assays were performed in purified brain cell nuclei to determine Parp activity by incorporation of radiolabeled ADP-ribose moieties from nicotinamide adenine dinucleotide (NAD+) into nuclear proteins.