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Research Article Open access CC BY 4.0

The Effect of Silymarin on Serum Concentration of Soluble Apoptosis Markers in β-Thalassemia Major Patients Receiving Desferrioxamine

Nafiseh Esmaeil, Marjan Gharagozloo, Behjat Moayedi, Milad Mirmoghtadaei, Mahdi Ghatreh Samani

Journal of Advances in Medical and Pharmaceutical Sciences · pp. 52–56 · Published 21 Nov 2014

10.9734/JAMPS/2015/12818

Abstract

Background: Despite appropriate chelation therapy with desferrioxamine, iron deposition in visceral organs causes tissue damage in thalassemia major patients. Excess iron can generate reactive oxygen species (ROS) that may lead to cell death and apoptosis. Therefore, antioxidants such as plant flavonoids can be an effective treatment to reduce ROS in thalassemia patients. Aims: In this study, we aimed to investigate the serum levels of apoptosis markers in β-thalassemia major patients treated with silymarin and desferrioxamine. Study Design: This study was a randomized, double-blind, placebo controlled 6-month clinical trial Place and Duration of Study: This clinical trial was carried out at Sayed-Al-Shohada clinic of thalassemia, Isfahan University of Medical Sciences, Iran, for 6-month between August 2009 and February 2010. Methodology: The patients were randomized into two groups: one group (A) received desferrioxamine and placebo and the other group (B) received a combination of desferrioxamine and silymarin. Serum levels of soluble apoptosis markers including soluble Fas (sCD95,sFas), sCD95 ligand (sCD95L,sFasL), sTNF receptor type 1 (sTNFR1), sTRAIL and cytochrome C, were measured before and after the trial in two groups of 40 thalassemia major patients using ELISA kits. Statistical analysis was performed using SPSS 15 version for windows program; results were expressed as mean ± standard deviation (SD) and significance set at P< 0.05. Results: There was no statistically significant difference between desferrioxamine group and combined therapy group in serum concentration of apoptosis markers, except for sTNFR1 level (which decreased from 0.16±0.12 to 0.11±0.10ng/ml) in the silymarin treatment group (P<0.05). Conclusion: Our observation of decreased circulating concentrations of sTNFR1 in silymarin-treated patients may reflect anti-inflammatory activity of silymarin in β-thalassemia major. The finding that silymarin treatment had no effect on the level of soluble apoptosis marker could be an evidence for safety of silymarin treatment in thalassemia major patients. However, measuring the membrane levels of these markers is necessary to validate these results, as they are not expressed equally in different tissues.  

Thalassemia desferrioxamine silymarin sTNFR1 sCD95 sTRAIL cytochrome C sCD95L Fas

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