If the colour in the wells is green or the colour change does not appear uniform, gently tap the plate to ensure thorough mixing. Read the optical density (OD) at 450 nm using a microtiter plate reader within 15 min. The same methodology was used to detect NO, GSSG, MDA, TOS, TAS, SOD, CAT, GSH-Px. All data were analysed using the Statistical

Package for the Social Sciences (SPSS) software, Statistics 17.0 (SPSS Inc., Chicago, IL, USA), and the data were presented as mean ± standard error of the mean (SEM). Statistical differences between the two groups were evaluated by analysis with Student’s t-test. A P-value <0.05 was considered statistically significant. Compared to healthy subjects, patients with chronic ITP showed significantly decreased levels of SOD, CAT, GSH-Px, GSH, TAS, (SOD, t = 10.08, P < 0.05; CAT, t = 5.82, P < 0.05; GSH-Px, t = 10.32, P < 0.05; GSH, EMD 1214063 t = 8.93, P < 0.05; TAS, t = 3.42, P < 0.05) in the peripheral blood (Table 2), but concentrations of NO, GSSG, MDA, TOS significantly increased (NO, t = 12.30,

P < 0.05; GSSG, t = 8.27, P < 0.05; MDA, t = 6.81, P < 0.05; TOS, t = 13.62, P < 0.05). Epacadostat nmr The difference between chronic ITP patients and healthy subjects was statistically significant (Fig. 1, Table 3). The correlation between contents of oxidant/antioxidant stress parameters and platelet count was assessed in patients with chronic ITP. Significant negative correlations were found between platelet count and NO (R = −0.6422,P = 0.0012), GSSG (R = −0.7794, P = 0.0007), MDA (R = −0.8326, P = 0.0002), TOS (R = −0.8315, P = 0.0002), respectively (Fig. 2 F,G,H,I). Meanwhile, significant positive correlations existed between platelet count and SOD (R = 0.8186, P = 0.0003), CAT (R = 0.8657, P = 0.0001), GSH-Px (R = 0.8321, P = 0.0002), GSH (R = 0.7795, P = 0.0006), TAS (R = 0.7711, P = 0.0007), respectively (Fig. 2A,B,C,D,E). Immune

thrombocytopenic purpura C-X-C chemokine receptor type 7 (CXCR-7) (ITP) is a common autoimmune disorder resulting in isolated thrombocytopenia. ITP can present either alone (primary) or in the setting of other conditions (secondary) such as infections or altered immune states. ITP is associated with a loss of immune tolerance to platelet antigens and a phenotype of accelerated platelet destruction and impaired platelet production [10]. Although the aetiology of ITP remains unknown, complex dysregulation of the immune system is observed in ITP patients. Antiplatelet antibodies mediate rapid clearance from the circulation in large part via the reticuloendothelial (monocytic phagocytic) system [11]. In addition, cellular immunity is perturbed and T cell and cytokine profiles are significantly shifted towards a type 1 and Th17 proinflammatory immune response [12]. The precise mechanism of the immune dysfunction, however, is generally not known. Until recently, no diagnostic criteria have been established, and the diagnosis is based on excluding other causes of thrombocytopenia.