Damage to endothelial cells is a key event in the pathogenesis of atherosclerosis and vascular disease. This study aimed to determine whether free fatty acids (FFAs) induced oxidative stress and apoptosis in human brain microvascular endothelial cells (HBMVECs) in vitro and, if so, which signalling pathway mediated these effects. After culture in different concentrations of FFAs for 24 - 72 h, cell viability/proliferation was determined using a cell counting kit, apoptosis was detected by measuring caspase-3 activity and by using annexin V-conjugated fluorescein isothiocyanate/propidium iodide staining, and oxidative stress was evaluated by measuring the levels of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP). The HBMVECs exposed to FFAs showed significantly decreased cell proliferation, increased apoptosis and ROS levels, and decreased MMP. In conclusion, the results showed that high levels of FFAs induced oxidative stress, which damaged HBMVECs and resulted in apoptosis.
The goal of this study is to examine a novel hypothesis that the progression of diabetes is partially due to the weakened survival of CD25high T cells, and prolonging survival of CD25high T cells inhibits the development of diabetes. Since CD28 co-stimulation is essential for the survival of CD4+CD25high T cells, we determined whether CD28-upregulated translationally controlled tumor protein (TCTP) prolongs the survival of CD4+CD25high regulatory T cells (Tregs) by a transgenic approach. The TCTP transgene prevents Tregs from undergoing apoptosis induced by Interleukin-2 withdrawal-, dexamethasone-, cyclophosphamide-, and anti-Fas treatment in vitro. In addition, transgenic Tregs express higher levels of FOXP3 than wild-type counterparts and maintain suppressive activity, suggesting that TCTP promotes Tregs escape from thymic negative selection, and that prolonged survival does not attenuate Treg suppression. Moreover, TCTP transgenic Tregs inhibit the development of autoimmune diabetes due to increased survival of suppressive Tregs and decreased expression of pancreatic TNF-α. Promoting the survival of CD25high T cells leads to prolonged survival of Tregs but not activated CD25+ non-Treg T cells. Thus, we propose a new model of “two phase survival” for Tregs. Our results suggest that modulation of Treg survival can be developed as a new therapy for autoimmune diseases.
Based on the importance of exercise and crucial role of liver in metabolism, the aim of this study was to determine whether the expression of peroxisome proliferator-activated receptor (PPAR)-α, γ and adiponectin receptor 2 in OLETF rat liver were altered in conjunction with improved metabolism with exercise training. OLETF rats were randomly assigned to 2 groups: sedentary control group (n=26), and long-term exercise-trained group (n=26). Full data were available on 32 OLETF rats (16 for each group). Adiponectin, glucose, insulin, triglyceride and cholesterol were assessed. Livers were taken to determine the expression of PPAR-α, γ and adiponectin receptor 2. Compared with sedentary control group, fasting glucose (9.38 ± 2.99 mmol/L vs. 7.32 ± 1.76 mmol/L, P<0.05), triglyceride (1.73 ± 0.34 mmol/L vs. 0.89 ± 0.12 mmol/L, P<0.05) and cholesterol (4.41 ± 0.75 mmol/L vs. 2.13 ± 0.32 mmol/L, P<0.05) were substantially reduced after exercise, which significantly correlated with increased PPAR-α (P<0.05) in liver. The expression of PPAR-α upstream and target genes, including hepatocyte nuclear factor-4 (HNF4), carnitine palmitoyl transferase 1 (CPT-1), catalase (CAT) and ATPbinding cassette transporter A1 (ABCA1) also increased significantly. Therefore, our findings suggest that increased PPAR-α expression in OLETF rats liver is a contributory factor to the exercise-related improvements in whole-body metabolism.
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