Résumé
Background: Carbon tetrachloride [CC14] is an industrial solvent that causes liver, kidneys, lungs, testis and brain as well as in blood diseases by generating free radicals. Previous studies on the chemical composition of S. pachycarpa have shown the presence of antioxidant compounds such as flavonoids
Objective: In the present study we investigated protective effects of Sophora pachycarpa extracts on serum level of sex hormones, urea and uric acid in carbon tetrachloride-intoxicated in male rats
Methods: Thirty six male wistar rats [195-200 g] were selected and randomly divided into 6 groups [n=6]: 3 pre-treatment groups received s.pachycarpa extract at doses 50 mg/kg/day, 100 mg/kg/day and 250 mg/kg/day by gavage for 21 days prior to intraperitoneal injection of CC14 500 micro/kg on 21[st] day, control group, CC14 group received 500 micro/kg CC14 on the 21[st] day, post-treatment group received extract at doses 100 mg/kg/day for 10 day at 12h after CCI4 250 micro/kg injection. At the end of the treatment, blood was collected by cardiac puncture from all of the animals and serum levels of sex hormones, urea and uric acid were assessed
Results: Serum levels of follicle stimulating hormone was significantly increased in serum of pre-treatment group III and serum level of luteinizing hormone and testosterone in serum of pre-treatment groups compared to CC14 was significantly increased [P<0.05]
Also serum levels of urea in pre-treatment and post-treatment groups and serum level of uric acid in serum of pre-treatment II and III [100 and 250 mg/kg] was significantly decreased compared to CC14 [P<0.05]
Conclusion: Together, our data suggest that Sophora pachycarpa extract can potentially ameliorate toxic effects of CCI4
Résumé
Evaluating the effect of DMSO concentrations on g-globin expression in Hu11 cells Asgharian AM1, Banan M2, Deilami Z1, Gharesouran J3, Ghasemi S4, Behjati F2, Javadi GR5, Kahrizi K6, Najmabadi H7 1 PhD Student of cell and molecular biology, Department of Biology, Islamic Azad University, Science and Research Branch, Tehran, Iran. 2 Assistant professor, Genetics Research Center, University of Social Welfare and Rehabilitation Sciences. Tehran, Iran. 3 Student of MSc of Genetics, Genetics Research Center, University of Social Welfare and Rehabilitation Sciences. Tehran, Iran. 4 MSc of Genetics,Genetics Research Center, University of Social Welfare and Rehabilitation Sciences. Tehran, Iran. 5 Associate Professor, Department of Biology, Islamic Azad University, Science and Research Campus, Tehran, Iran. 6 Associate Professor, Genetics Research Center, University of Social Welfare and Rehabilitation Sciences. Tehran, Iran. 7 Professor, Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran Abstract Background: Understanding of the mechanisms involved in gamma- to beta-globin switching may be important for development of treatment options for b-thalassemia. Such studies require the availability of relevant cellular model systems. One such cell type is Hu11, a mouse erythroleukemia [MEL] cell line containing the human b-locus. MEL and Hu11 cells differentiate in the presence of the chemical dimethyl sulfoxide [DMSO]. Nevertheless, levels of gamma-globin induction in Hu11 cells after DMSO treatment have not been determined. In the present study, we determined gamma-globin levels in Hu11 cells after treatment with various DMSO concentrations. Materials and methods: Hu11 cells were cultivated in various DMSO concentrations and the levels of gamma-globin were determined by real-time PCR. Results: Our study showed that hemoglobin in Hu11 cells treated with 1% and 2% DMSO was increased by approximately 5 and 10 folds. Moreover real-time PCR results showed that g-globin levels using the indicated DMSO levels were increased by 66 and 298 folds, respectively. Hu11 cells differentiate in the presence of DMSO, and in doing so, their gamma-globin levels are increased. Therefore these cells can be used to study the mechanisms of gamma-globin induction. Such studies may be beneficial for the treatment of beta-thalassemia