Protective effects of black cumin (Nigella sativa) oil on TNBS-induced experimental colitis in rats.

BACKGROUND: The pathogenesis and treatment of ulcerative colitis remain poorly understood. The aim of the present study is to investigate the effects of black cumin (Nigella sativa) oil on rats with colitis. METHODS: Experimental colitis was induced with 1 mL trinitrobenzene sulfonic acid (TNBS) in 40% ethanol by intracolonic administration with 8-cm-long cannula under ether anesthesia to rats in colitis group and colitis + black cumin oil group. Rats in the control group were given saline at the same volume by intracolonic administration. Black cumin oil (BCO, Origo "100% natural Black Cumin Seed Oil," Turkey) was given to colitis + black cumin oil group by oral administration during 3 days, 5 min after colitis induction. Saline was given to control and colitis groups at the same volume by oral administration. At the end of the experiment, macroscopic lesions were scored and the degree of oxidant damage was evaluated by colonic total protein, sialic acid, malondialdehyde, and glutathione levels, collagen content, and tissue factor, superoxide dismutase, and myeloperoxidase activities. Tissues were also examined by histological and cytological analysis. Proinflammatory cytokines [tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1ß, and IL-6], lactate dehydrogenase activity, and triglyceride and cholesterol levels were analyzed in blood samples. RESULTS: We found that black cumin oil decreased the proinflammatory cytokines, lactate dehydrogenase, triglyceride, and cholesterol, which were increased in colitis. CONCLUSIONS: BCO, by preventing inflammatory status in the blood, partly protected colonic tissue against experimental ulcerative colitis.

Pancreatic islet derived stem cells can express co-stimulatory molecules of antigen-presenting cells.

BACKGROUND: Antigen-presenting cells (APCs) are crucial intermediates in the generation of both innate and specific immune responses. It has long been understood that some APCs are resident in islets in situ as well as after isolation. Our aim was to investigate the presence of molecules involved in antigen presentation in rat pancreatic islet-derived stem cells (PI-SCs). METHODS: We used immunocytochemistry and reverse transcription polymerization chain reaction to study immunophenotypic characteristics; pluripotent-related gene expressions; transcripts coding for antigen-presenting surface proteins CD40, CD80, CD86; and major histocompatibility complex class II in addition to genes with known antiapoptotic functions including mitogen-activated protein kinase-activated protein kinase 2 (MAPKAPK2), tumor necrosis factor alpha-induced protein 3 (TNFAIP3) interacting protein 1 (TNIP1) and BCL3 of the PI-SCs. RESULTS: Rat PI-SCs were negative for CD45 as demonstrated by flow cytometry and for CD31, CD34, and CD71 as demonstrated by immunocytochemistry. Therefore, there was no evidence of hematopoietic precursors in the cultures. OCT4, SOX2, and REX1 were expressed by rat PI-SCs. We determined the expression of genes for antigen-presenting surface proteins CD40 and CD80, and genes with known antiapoptotic functions including MAPKAPK2, TNIP1 and BCL3, besides the surface protein, CD80, by flow cytometry. CONCLUSION: Expression of these genes by rat PI-SCs implied that they could be involved in the regulation of immunity in islets, highlighting the influence of protective role-playing antiapoptotic mechanisms on pancreatic islet cells. This study offers the potential to understand the molecular mechanisms of a devastating disease, type-1 diabetes mellitus.

Protection of rat pancreatic islet function and viability by coculture with rat bone marrow-derived mesenchymal stem cells.

The maintenance of viable and functional islets is critical in successful pancreatic islet transplantation from cadaveric sources. During the isolation procedure, islets are exposed to a number of insults including ischemia, oxidative stress and cytokine injury that cause a reduction in the recovered viable islet mass. A novel approach was designed in which streptozotocin (STZ)-damaged rat pancreatic islets (rPIs) were indirectly cocultured with rat bone marrow-derived mesenchymal stem cells (rBM-MSCs) to maintain survival of the cultured rPIs. The results indicated that islets cocultured with rBM-MSCs secreted an increased level of insulin after 14 days, whereas non-cocultured islets gradually deteriorated and cell death occurred. The cocultivation of rBM-MSCs with islets and STZ-damaged islets showed the expression of IL6 and transforming growth factor-ß1 in the culture medium, besides the expression of the antiapoptotic genes (Mapkapk2, Tnip1 and Bcl3), implying the cytoprotective, anti-inflammatory and antiapoptotic effects of rBM-SCs through paracrine actions.

Effect of copper on liver and bone metabolism in malnutrition.

This study was planned to investigate the effects of copper (Cu) deficiency on liver and bone metabolism in malnourished children. Serum total calcium (Ca), inorganic phosphorus (P), Ca/P, Cu/Ca, Cu/P ratios and alkaline phosphatase (ALP) activity values were analyzed. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyltransferase (GGT) enzyme activities and the ALT/AST (De Ritis) ratio as well as their correlations with Cu were tested to determine liver function. The results of the study showed that Cu deficiency directly affects the organic matrix formation, and by the suppression of ALP activity, indirectly causes decalcification. In the liver, however, no direct effect of Cu deficiency was seen. Deterioration in liver function and Cu deficiency increased parallel with the severity of malnutrition. Thus we concluded that a correlation exists between Cu and the parameters that indicate liver function.