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    Category: Peer Reviewed Papers

    Effects of Cacao Flavonoids in Long COVID-19 Patients with Chronic Fatigue: FLALOC, a Placebo-Controlled Randomized Clinical Trial

    Abstract Background: In the context of long COVID, persistent fatigue is among the most prevalent symptoms that can develop after SARS-CoV-2 infection. Mitochondrial myopathy and endothelial dysfunction, which are triggers of inflammation, have emerged as prominent causes of long COVID-induced fatigue. Interestingly, the intake of flavanols, particularly (−)-epicatechin (EC), has been associated with the positive modulation of endothelial and mitochondrial structure and function. Methods: In this work, we conducted a randomized, double-blind, placebo-controlled clinical trial to determine whether an EC-enriched supplement (ECES) improves plasma markers of inflammation, endothelial structure, and fatigue-related endpoints in patients with long COVID-19. Results: The study included 46 subjects (mean age 52 years) who were instructed to consume two capsules/day for 90 days of either ECES (n = 23) or placebo (n = 23). Endpoints assessed included mean changes in plasma inflammatory markers (IL-1β, IL-6, and TNF-α) and endothelial dysfunction markers (syndecan-1), handgrip strength, fatigue scale, and quality of life (QoL). The results showed significant improvements in the ECES group for inflammatory markers, syndecan-1, and fatigue compared with the placebo group. Conclusions: The results yield intriguing positive findings for EC and open a new avenue for treating long COVID.

    Anticancer potential of (−)-epicatechin in a triple-negative mammary gland model

    Objectives The main aim of this work was to analyse the potential tumour growth inhibition effects of (−)-epicatechin (EC). Triple-negative breast cancer (TNBC) is an invasive form of cancer characterized by the absence of progesterone receptor, estrogen receptor and human epidermal growth factor receptor 2. Doxorubicin (DOX) is widely used for its anti-tumour activity. EC belongs to the flavanol subfamily and is a candidate molecule for the adjuvant treatment of cancer due to its antiproliferative activities.

    Characterization Of The Cytotoxic Effects Of The Combination Of Cisplatin And Flavanol (-)-Epicatechin On Human Lung Cancer Cell Line A549. An Isobolographic Approach

    Background: Among malignancies, lung cancer is a leading cause of death. Platinum-based therapeutic compounds used to treatlung cancer have not been able to increase the survival of patients and such compounds have a high incidence of adverse and toxiceffects. It has been proposed that flavonoids such as catechins may significantly reduce the risk of developing cancer, alongsidewith other health benefits. The aim of this work was to determine the effect of (-)-epicatechin, the main flavanol found in cocoa,on the proliferation of the lung non-small cell adenocarcinoma cancer cell line A549, and to determine its effects when added simultaneously with cisplatin. Materials and Methods: Concentration-response curves for cisplatin and epicatechin were obtained,inhibitory concentrations calculated and an isobolographic analysis was then performed. Results: We found that epicatechin hasa concentration-dependent inhibitory effect on proliferation of tumor cells and the isobolographic analysis reveals that the effectof its combination with cisplatin is synergistic. It was also observed that epicatechin promotes cell death by apoptosis. Conclusions:Epicatechin might be considered for future studies to explore its possible use as coadjuvant in cisplatin-based treatments.Key Words: epicatechin, lung cancer cells, cisplatin, isobologram.

    Epicatechin limits renal injury by mitochondrial protection in cisplatin nephropathy

    Abstract: Cisplatin nephropathy can be regarded as a mitochondrial disease. Intervention to halt such deleterious injury is under investigation. Recently, the flavanol (–)-epicatechin emerges as a novel compound to protect the cardiovascular system, owing in part to mitochondrial protection. Here, we have hypothesized that epicatechin prevents the progression of cisplatin-induced kidney injury by protecting mitochondria. Epicatechin was administered 8 h after cisplatin injury was induced in the mouse kidney. Cisplatin significantly induced renal dysfunction and tubular injury along with an increase in oxidative stress. Mitochondrial damages were also evident as a decrease in loss of mitochondrial mass with a reduction in the oxidative phosphorylation complexes and low levels of MnSOD. The renal damages and mitochondrial injuries were significantly prevented by epicatechin treatment. Consistent with these observations, an in vitro study using cultured mouse proximal tubular cells demonstrated that cisplatin-induced mitochondrial injury, as revealed by a decrease in mitochondrial succinate dehydrogenase activity, an induction of cytochrome c release, mitochondrial fragmentation, and a reduction in complex IV protein, was prevented by epicatechin. Such a protective effect of epicatechin might be attributed to decreased oxidative stress and reduced ERK activity. Finally, we confirmed that epicatechin did not perturb the anticancer effect of cisplatin in HeLa cells. In conclusion, epicatechin exhibits protective effects due in part to its ability to prevent the progression of mitochondrial injury in mouse cisplatin nephropathy. Epicatechin may be a novel option to treat renal disorders associated with mitochondrial dysfunction.