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Proteomic analysis of plasma protein in β‐thalassemia/HbE patients treated with curcumin
Author(s) -
Kalpravidh Ruchaneekorn,
Weeraphan Churat,
Srisomsap Chantragan,
Siritanaratkul Noppadol,
Svasti M.R. Jisnuson
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.858.1
Subject(s) - curcumin , hemopexin , haptoglobin , fibrinogen , oxidative stress , hemostasis , medicine , thalassemia , blood proteins , chemistry , coagulation , antioxidant , pharmacology , endocrinology , biochemistry , heme , enzyme
Thalassemia is a group of genetic disorders resulting from different mutations in the globin gene clusters and leading to an imbalance in globin synthesis. Unpaired globin chains are less stable and are susceptible to oxidation. Patients with beta‐thalassemia/HbE (β‐thal/HbE) are prone to increase oxidative stress as indicated by increased lipid peroxidation and protein oxidation. Curcumin, a strong antioxidant and iron chelator, has been shown to decrease oxidative stress in β‐thal/HbE patients. In this study, the effect of curcumin on plasma protein expression was investigated using proteomic analysis in untreated patients as compared to normal subjects and in patients before and after supplementing with 500 mg curcumin daily for 12 months. Plasma proteins involved in blood coagulation and hemostasis e.g. prothrombin, fibrinogen, hemopexin, and haptoglobin were significantly decreased in patients, particularly in splenectomized patients. The administration of curcumin led to significant increase of prothrombin, fibrinogen, and haptoglobin. Our results provide strong evidence for the existence of a chronic hypercoagulable state in thalassemia and the patients responded to curcumin supplement as shown by a rise in the level of procoagulant proteins. Therefore, the administration of curcumin could be beneficial for thalassemic patients as adjunct therapy to decrease hypercoagulable state.