RESUMEN
Purpose: Diabetes Mellitus (DM) is a systemic disease that can effect tissues and their physiological functions at molecular and biochemical levels. Diabetic osteoporosis is one of the chronic diseases of bone metabolism effected by and characterized by augmented risk of osteoporotic fractures and destroying of bone microarchitecture. It was aimed to investigate the alterations in femoral bone structure that may take place as a complication of DM by using the antioxidant properties of eugenol and quercetin, which are phenolic compounds, in streptozotocin nicotinamide (STZ-NA) induced rats as an experimental type 2 DM (T2 DM) model. Methods: The antioxidant effect of eugenol and quercetin in case of DM development was determined by GSH ELISA kit. The effect of DM on alterations in bone structure was analyzed by micro CT. BMD, Tb.Bv/Tb.Tv, Tb.N, Tb.Th, Ct.Th, Tb.Sp and SMI data were calculated with the software CTAn. Results: Serum GSH levels, Tb.Th and Tb.Bv/Tb.Tv values statistically decreased, and SMI values statistically increased in diabetic group compared with controls. Serum GSH levels in eugenol group were higher than diabetic group, and Tb.Bv/Tb.Tv values in eugenol group were lower than controls. Quercetin group had higher serum GSH levels and Tb.Th values compared with diabetic group, while SMI values were lower in quercetin group compared with diabetic group. Conclusion: Eugenol and quercetin were revealed to have antioxidant, antidiabetic and osteoprotective effects on the repair of bone structure in experimental STZ-NA T2 DM model.
RESUMEN
The aim of this study was to investigate changes in primitive hematopoietic cells through CD38 expression, identify the stage at which erythrocyte differentiation CD38 gains activity and the effects of serum factors on this expression by establishing a hematopoietic stem cell system in the erythroid development process. Using an immunomagnetic labeling and separation technique, CD34(+) cells were selected from cord blood. The CD34(+) cells were cultured in a 2 mM L-glutamine-enriched medium containing erythropoietin (Epo), penicillin-streptomycin and stem cell factor (SCF), and were incubated in 5% CO(2) at 37°C. In erythroid development pathways following CD38 expression, primitive/progenitor human hematopoietic cells obtained from cord blood were assessed through the erythroid development process in a serum-free medium in the presence of proper SCF and Epo. At the end of the 26-day process, using staining with a Megacult-c staining kit, it was determined that progenitor cells nucleate and differentiate into erythroid cell lines of 8-10 µm. During the course of this process, we analyzed increases over time in NAD glycohydrolase activity rates using the supernatant liquid samples. Results of co-culture experiments in cell culture studies showed that the stimulating effects of CD38 expression originate from specific serum factors. CD38 expression has been shown to occur at hematopoietic cell sources as well as at a number of differentiation levels. In the proliferation process the possible induction of CD38 through specific serum factors leads us to conclude that it may be involved in proliferation with a physiological task or that it may be involved in an event, such as an apoptotic process.
RESUMEN
Erythrocyte and lymphocyte NAD(+) glycohydrolase levels were previously found to be elevated in cancer patients. These results were confirmed in an animal model. The administration of live Ehrlich ascites tumor cells to BALB/c mice led to increases in erythrocyte and lymphocyte NAD(+) glycohydrolase, along with tumor development. Serum samples, ascites fluid from mice with developed tumors, serum samples from cancer patients and Ehrlich cell supernatants had a similar stimulatory effect when administered to mice or when incubated with peripheric lymphocytes in culture. These increases were accompanied by the appearance of an anti-CD38 reactive band of 45 kDa in SDS-PAGE/Western blot analyses of erythrocyte ghost and lymphocyte membrane proteins. The results, supported by flow cytometry data, support previous clinical findings that an enhancement in CD38 expression occurs in the hematopoietic system during proliferative processes. Moreover, they suggest that CD38 expression is triggered at least in part by a certain cytokine(s) secreted by cancer cells. Finally, the results emphasize the prospective use of CD38 expression as a marker of tumor development and progression.