Abstract: The aim of the study was to investigate the protective effects of sodium hydrosulfide (NaHS), a H2S donor, against hypoxia-induced injury in human umbilical vein endothelial cells (HUVECs) and also to look into the possible mechanisms by which H2S exerts this protective effect. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and scratch wound healing assay were chosen to measure the cell viability and migration-promoting effects. The fluorescent probe, DCFH-DA and 5,5',6,6'-Tetrachloro-1,1',3,3'-tetraethyl-imidacarbocyanine iodide (JC-1) were applied to detect the reactive oxygen species (ROS) level and mitochondrial membrane potential (ΔΨm). Furthermore, western blots were used to measure the expressions of the apoptosis-related proteins. Under hypoxic conditions, 300 μM and 600 μM of H2S could protect HUVECs against hypoxia-induced injury, as determined by MTT assay. Following the treatment of 60 µM NaHS for 18 h, scratch wound healing assays indicated that the scratch became much narrower than control group. After treatment with 60 µM, 120 µM, and 600 µM NaHS, and hypoxia for 30 min, flow cytometry demonstrated that the ROS concentrations decreased to 95.08 % ± 5.52%, 73.14 % ± 3.36%, and 73.51 % ± 3.05%,

Abstract: High Density Lipoprotein (HDL) has been witnessed to possess a range of different functions that contribute to its atheroprotective effects. These functions are: the promotion of macrophage cholesterol efflux, reverse cholesterol transport, anti-inflammatory, anti-thrombotic, anti-apoptotic, pro-fibrinolytic and anti-oxidative functions. Paraoxonase 1 (PON1) is an HDL associated enzyme esterase/homocysteinethiolactonase that contributes to the anti-oxidant and anti-atherosclerotic capabilities of HDL. PON1 is directly involved in the etiopathogenesis of atherosclerosis through the modulation of nitric oxide (NO) bioavailability. The aim of this review is to summarize the role of HDL on endothelial homeostasis, and also to describe the recently characterized molecular pathways involved. Keywords:, Endothelial function, high-density lipoprotein, homocysteine, nitric oxide, oxLDL, oxidative stress, paraoxonase.

Endothelial dysfunction: are we ready to heed the vasculature’s early-warning signal? hANS STRIJDOM Endothelial dysfunction (ED) refers to a spectrum of pathophysiological changes in the vascular endothelium that ultimately results in a loss of vascular homeostasis. Traditional cardiovascular risk factors (e.g. diabetes mellitus, smoking, dyslipidaemia and hypertension) are all associated with the development of ED via sustained and harmful effects, mediated by circulating stimuli such as pro-inflammatory tumour necrosis factor-alpha (TNF-alpha), oxidised low-density lipoprotein (ox-LDL), asymmetrical dimethyl-arginine (ADMA), angiotensin II and hyperglycaemia.1 The underlying cellular mechanisms of ED are directly or indirectly related to the development of oxidative stress (particularly increased superoxide anion production via NADPH-oxidase and xanthine oxidase), which reduces the bioavailability of the main endothelial-derived vasodilator, nitric oxide (NO) via the reaction of superoxide with NO (thereby scavenging NO) to form peroxynitrite (ONOO-), a highly reactive molecule. The latter has the ability to uncouple endothelial NO synthase (eNOS), which further reduces NO production and simultaneously increases superoxide anion generation.2 As a result, vascular endothelial function becomes compromised, manifesting as a loss of endothelium-dependent vasorelaxation, increased thrombosis, the development of a generalised pro-inflammatory state (increased expression of vascular adhesion molecules) and increased vascular permeability.3 Ultimately, ED can develop into atherosclerosis.2 The importance of ED as a potential predictor of long-term development of atherosclerosis and cardiovascular event rate2 is evident by the high number of research articles on this topic

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