RESUMO
Anthocyanins (ACNs) are phytochemicals with numerous bioactivities, e.g., antioxidant and anti-inflammatory. Health benefits from consuming ACN-rich foods, extracts, and supplements have been studied in clinical trials (CT). However, the individual effect of single ACNs and their correlation with doses and specific bioactivities or molecular targets have not been thoroughly analyzed. This review shows a recompilation of single anthocyanins composition and concentrations used in CT, conducted to investigate the effect of these anti-inflammatory derivatives in obese condition. Single anthocyanin doses with changes in the levels of frequently monitored markers were correlated. In addition, the analysis was complemented with reports of studies made in vitro with single ACNs. Anthocyanins' efficacy in diseases with high baseline obesity-related inflammation markers was evidenced. A poor correlation was found between most single anthocyanin doses and level changes of commonly monitored markers. Correlations between cyanidin, delphinidin, and pelargonidin derivatives and specific molecular targets were proposed. Our analysis showed that knowledge of specific compositions and anthocyanin concentrations determined in future studies would provide more information about mechanisms of action.
RESUMO
Obesity leads to chronic oxidative stress promoting the development of cardiovascular diseases including coronary artery disease and endothelial dysfunction. Increased reactive oxygen species production associated with obesity might lead to endothelial dysfunction through cyclooxygenase (COX) pathway. We evaluated arachidonic acid (AA)-dependent coronary vascular responses and explored COX metabolism in obese C57BL/6 mice. In response to arachidonic acid (AA), isolated hearts from obese mice showed increased vasoconstriction compared with control mice. Released thromboxane (TX) A2 during AA-induced vasoconstriction phase was increased in heart perfusates from obese mice. Indomethacin and 1-benzylimidazole, both reduced vasoconstriction response in control and obese mice. Vasoconstriction response to TXA2 mimetic analog U46619 was 2.7 higher in obese mice. Obesity increased COX-2, TXS and TX receptor protein expression as well as oxidative stress evaluated by nitrotyrosine and peroxynitrite levels, compared with control mice. Obese mice treated with FeTMPyP, a peroxynitrite scavenger, reversed all these parameters to control levels. These data suggest that alterations in COX pathway may be associated with increased generation of free radicals, including peroxynitrite, that result from the oxidative stress observed in obesity.