Abstract: Background: Physical exercise induces a pattern of hormonal and immunological responses that prevent endothelial dysfunction by maintaining the availability of nitric oxide (NO). Regular and moderate exercise stimulates NO release, that can be considered as protective factor of cardiovascular diseases, while strenuous exercise induces increased levels in a number of pro-inflammatory and anti-inflammatory cytokines. Pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) triggers endothelial activation which results in an increased vascular permeability. Nuclear gene factor kappa B (NF-κB) activates biological effect of TNF-α. Aim of Study: To determine the effect of physical exercise on the endothelial and skeletal muscle, we measured the level of NF-κB on rats’ serum, macrophages, and myocytes after strenuous physical exercise. Methods: 30 male Rattus norvegicus in the age of eight weeks were randomly divided into five groups (each containing six), and there were treated groups (T) and control group (C). The treated groups obtain strenuous physical exercise by ran on treadmill at 32 m/minutes for 1 hour or until exhaustion. Blood samples, myocytes of gastrocnemius muscle, and intraperitoneal macrophages were collected sequentially. There were investigated immediately, 2 hours, 6 hours, and 24 hours (T1, T2, T3, and T4) after sacrifice. The levels of NF-κB were measured by ELISA methods. Results: From our study, we found that the levels of NF-κB on myocytes in treated group from which its specimen was taken immediately (T1), 2 hours after treadmill (T2), and 6 hours after treadmill (T3) were significantly higher than control group (p0.05). Also on macrophages, NF-κB in treated groups T1, T2, and T3 was significantly higher than control group (p0.05). The level of serum NF-κB was not significantly different between treatment group as well as compared to control group (p>0.05). Serum NF-κB was significantly higher than the level on macrophages and myocytes (p
Abstract: Hyperglycaemia is a key factor that contributes to the
development of diabetes-related microvascular disease and a major
risk factor for endothelial dysfunction. In the current study, we have
explored glucose-induced abnormal intracellular calcium (Ca2+
i)
homeostasis in mouse microvessel endothelial cells (MMECs) in
high glucose (HG) (40mmol/L) versus control (low glucose, LG) (11
mmol/L). We demonstrated that the exposure of MMECs to HG for 3
days did not change basal Ca2+
i, however, there was a significant
increase of acetylcholine-induced Ca2+ entry. Western blots
illustrated that exposure to HG also increased STIM1 (Stromal
Interaction Molecule 1), but not Orai1 (the pore forming subunit),
protein expression levels. Although the link between HG-induced
changes in STIM1 expression, enhanced Ca2+ entry and endothelial
dysfunction requires further study, the current data are suggestive
that targeting these pathways may reduce the impact of HG on
endothelial function.