Epicatechin as a modulator of mitochondrial function in THP-1 lineage monocytes

Public health problems are increasingly prevalent worldwide, and many diseases have a multifactorial nature and complex pathophysiology. In this context, mitochondrial dysfunction has emerged as a recent target of investigation, being observed in several conditions such as neurodegenerative and metabolic diseases, highlighting the complexity of their treatment. Given this scenario, the search for new therapeutic alternatives that act at the mitochondrial level represents an important focus of research. Epicatechin (EC), a flavonoid found in various plants, possesses well-known beneficial biological properties. This study aims to analyze the effects of EC in reversing mitochondrial damage induced by known oxidative agents. THP-1 monocyte cell lines were exposed to rotenone, sodium azide, or sodium nitroprusside and subsequently treated with epicatechin. Assays were performed to evaluate cell viability, reactive oxygen species (ROS) production, nitric oxide release, the presence of extracellular double-stranded DNA (dsDNA), and DNA damage through the alkaline comet assay. The results are consistent with the literature and indicate that, at certain concentrations, EC can attenuate the induced damage in the evaluated parameters, demonstrating potential as a cellular protective agent. Thus, EC shows the ability to protect cells and minimize mitochondrial damage, highlighting its promise as a therapeutic candidate for further investigation.