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Objective@#Specific learning disorder (SLD) is a neurodevelopmental disorder in which underlying pathogenesis and etiological factors are not fully understood. Neuroinflammatory response (measured with serum levels of galectin-1 and galectin-3), which is associated with learning and memory, may play an important role in the etiopathogenesis of SLD. Aim of the present study is to examine whether serum galectin-1 and galectin-3 levels are related to SLD. @*Methods@#The current study consisted of 42 treatment-naive children with SLD and 42 control subjects. All of the subjects were assessed using semi-structured psychiatric examination to diagnose SLD and exclude attention-deficit hyperactivity disorder. Serum galectin-1 and galectin-3 levels were measured via venous blood samples. @*Results@#The SLD and control group did not differ significantly in terms of age, sex, and body mass index (BMI). The SLD group had significantly higher serum levels of galectin-1 (8.78±2.97 vs. 7.40±2.03, p=0.019) and galectin-3 (1.86±0.93 vs. 1.32±0.69, p=0.003) than the control group when controlled for age, sex, and BMI. @*Conclusion@#Higher serum levels of galectin-1 and galectin-3 in children with SLD may indicate the role of neuroinflammatory response in the pathogenesis of SLD. Other mechanisms involving galectin-1 and galectin-3 related to learning may play a part in the etiology of SLD.
RESUMO
Objective: The imbalance in oxidant/antioxidant status plays a pivotal role in diabetes mellitus [DM]. Selenium is a integral component of the antioxidant enzyme glutathione peroxidase. Se treatment induces angiogenesis and improves endothelial function through increased expression of vascular endothelial growth factor [VEGF]. The aim of this study is to investigate the effect of selenium on oxidative stress, VEGF, and endothelin 1 [ET1] in a DM rat model
Materials and Methods: We performed an experimental animal study with 64 adult male Wistar-Albino rats. Rats were divided into the following groups [n=8]: control [C]7, C21, C+sodium selenite [Se]7, and C+Se21 [control rats], and DM7, DM21, DM+Se7, and DM+Se21 [diabetic rats]. Diabetes was induced by 2-deoxy-2-[3-methyl-3-nitrosoureido]- D-glucopyranose [streptozotocin [STZ]]. Three weeks after STZ, DM+Se7 rats received intraperitoneal [i.p.] injections of 0.4 mg/kg Se for 7 days. The DM+Se21 rats received these injections for 21 days. The same dose/duration of Se was administered to the C+Se7 and C+Se21 groups. The remaining rats [C7, C21, DM7, DM21] received physi- ologic saline injections for 7 or 21 days. Ferric reducing antioxidant power [FRAP], malon- dialdehyde [MDA], advanced oxidation protein products [AOPP], and endothelial function markers [VEGF and ET1] in plasma samples were measured
Results: Diabetic rats [DM7 and DM21] had significantly increased plasma FRAP [P=0.002, P=0.001], AOPP [P=0.024, P=0.01], MDA [P=0.004, P=0.001], and ET1 [P=0.028, P=0.003] levels compared with C7 and C21 control rats. VEGF [P=0.02, P=0.01] significantly decreased in DM7 and DM21 diabetic rats compared with their controls [C7, C21]. Se administration reversed the increased MDA and decreased VEGF levels, and lowered plasma glucose levels in the DM+Se7 and DM+Se21 diabetic groups compared with diabetic rats [DM7, DM21]. We observed positive correlations between FRAP-AOPP [r=0.460], FRAP-ET1 [r=0.510], AOPP-MDA [r=0.270], and AOPP-ET1 [r=0.407], and a negative correlation between MDA-VEGF [r=-0.314]
Conclusion: We observed accentuated oxidative stress and impaired endothelial function in diabetes. Se treatment reduced lipid peroxidation and hyperglycemia. Se probably improved endothelial dysfunction in diabetic rats because of the increased VEGF levels