Effects of interventions on oxidative stress and inflammation of cardiovascular diseases

Abstract

Excessive oxidative stress and low-grade chronic inflammation are major pathophysiological factors contributing to the development of cardiovascular diseases (CVD) such as hypertension, diabetes and atherosclerosis. Accumulating evidence suggests that a compromised antioxidant system can lead to excessive oxidative stress in cardiovascular related organs, resulting in cell damage and death. In addition, increased circulating levels of pro-inflammatory cytokines, such as tumor necrosis factor α, interleukin-6 and C-reactive protein, are closely related to morbidity and mortality of cardiovascular complications. Emerging evidence suggests that interventions including nutrition, pharmacology and exercise may activate expression of cellular anti-oxidant systems via the nuclear factor erythroid 2-related factor 2-Kelchlike ECH-associated protein 1 signaling pathway and play a role in preventing inflammatory processes in CVD. The focus of the present review is to summarize recent evidence showing the role of these anti-oxidant and anti-inflammatory interventions in cardiovascular disease. We believe that these findings may prompt new effective pathogenesis-oriented interventions, based on the exercise-induced protection from disease in the cardiovascular system, aimed at targeting oxidant stress and inflammation.

Astaxanthin Decreases Inflammatory Biomarkers Associated with Cardiovascular Disease in Human Umbilical Vein Endothelial Cells

“…Certain conditions and lifestyle factors can greatly increase ones risk of developing CVD. While the relationships between these factors are complex, oxidative stress and inflammation are strongly linked to the development of CVD (Lee et al, 2011a). Despite this connection, there are few therapeutic interventions that successfully address this relationship between oxidative stress and CVD (Pashkow et al, 2008).…”

“…Under normal conditions, ROS concentrations are tightly controlled by endogenous antioxidant systems, including superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase. However, when endogenous antioxidants are overwhelmed by the overproduction of ROS, oxidative stress occurs resulting in inflammation and cellular damage (Lee et al, 2011a), thereby requiring dietary antioxidants to help scavenge these harmful molecules. Therefore, dietary antioxidants may play a beneficial role in treating CVD as they scavenge ROS and slow the progression of oxidative damage.…”

Influência do exercício físico nas alterações cardiovasculares induzidas pelo hipotireoidismo

“…Em humanos também já foi demonstrado que concentrações séricas de malondialdeído estavam significativamente aumentadas tanto em hipotireoideos subclínicos quanto clínicos. (24) Embora estudos mostrem que o exercício físico é capaz de retardar a formação de radicais livres, aumentar a produção de antioxidantes endógenos e reduzir o estresse oxidativo nas doenças cardiovasculares como a hipertensão, diabetes e aterosclerose (52)(53) , dados analisando seus efeitos sobre o estresse oxidativo em sujeitos com hipotireoidismo não foram encontrados mediante os critérios adotados para a seleção dos manuscritos.…”

Parametric Determination of Hypoxic Ischemia in Evolution of Atherogenesis

“…This is well-testified by smooth muscle cells that synthesize and secrete matrix proteoglycans, and oxidative stress also induces production of superoxide by endothelial cells with nitric oxide synthase uncoupling (Zweier et al, 2011). Significant participation in atherogenesis involves mirror-imaged targeting of multiple component systems within the vessel wall that developmentally integrate as regions of hypoxia and ischemia, including the thioredoxin system that correlates with cellular apoptosis in endothelial cell lines in hypoxic stress (Park et al, 2011). Neovascularization proves a permissive phenomenon in development of gradients of ischemia that redefine the individual plaque as compounding parameters of progression to further injury to the vascular wall.…”