Coffee leaf tea is prepared as an infusion of dried leaves of Coffea spp. in hot water. It is a traditional beverage in some coffee-producing countries and has been authorized in 2020 within the European Union (EU) according to its novel food regulation. This article reviews current knowledge on the safety of coffee leaf tea. From the various ingredients contained in coffee leaves, only two were highlighted as possibly hazardous to human health, namely, caffeine and epigallocatechin gallate (EGCG), with maximum limits implemented in EU legislation, which is why this article focuses on these two substances. While the caffeine content is comparable to that of roasted coffee beans and subject to strong fluctuations in relation to the age of the leaves, climate, coffee species, and variety, a maximum of 1–3 cups per day may be recommended. The EGCG content is typically absent or below the intake of 800 mg/day classified as hepatotoxic by the European Food Safety Authority (EFSA), so this compound is suggested as toxicologically uncritical. Depending on selection and processing (age of the leaves, drying, fermentation, roasting, etc.), coffee leaf tea may exhibit a wide variety of flavors, and its full potential is currently almost unexplored. As a coffee by-product, it is certainly interesting to increase the income of coffee farmers. Our review has shown that coffee leaf tea is not assumed to exhibit risks for the consumer, apart from the well-known risk of caffeine inherent to all coffee-related beverages. This conclusion is corroborated by the history of its safe use in several countries around the world.

Background: Lung dysfunction constitutes a severe complication after major cardiac surgery with cardiopulmonary bypass (CPB), substantially contributing to postoperative morbidity and mortality. The current possibilities of preventive and therapeutic interventions, however, remain insufficient. We, therefore, investigated the effects of intraoperative application of the antioxidant and anti-inflammatory green tea polyphenol epigallocatechin-3-gallate (EGCG) on CPB-associated lung injury. Materials and methods: Thirty piglets (8 - 15 kg) were divided into four groups: sham-operated and saline-treated control group (n = 7); sham-operated and EGCG-treated control group (EGCG-control group; n = 7); CPB group (n = 10); and CPB + EGCG group (n = 6). The CPB groups underwent 120 min of CPB followed by 90 min of recovery time. In the CPB + EGCG group, EGCG (10 mg/kg body weight) was administered intravenously before and after CPB. Hemodynamic monitoring, blood gas analysis, hematoxylin-eosin staining, and immunohistochemistry of lung tissue were performed. Results: Histologic examination revealed thickening of the alveolar wall and enhanced alveolar neutrophil infiltration in the CPB group (P < 0.05) compared with those in the control group, which was prevented by EGCG (P < 0.05). In the CPB group, higher formation of poly(ADP-ribose) and nuclear translocation of apoptosis-inducing factor were detected in comparison with those in the control group (P < 0.001), which were both reduced in the CPB + EGCG group (P < 0.001). Compared with the control group, the EGCG-control group showed thickening of the alveolar wall and increased neutrophil infiltration (P < 0.05). Conclusions: CPB leads to lung edema, pulmonary neutrophil infiltration, and presumably initiation of poly(ADP-ribose) polymerase-dependent cell death signaling in the lung. EGCG appears to attenuate CPB-associated lung injury, suggesting that this may provide a novel pharmacologic approach.

L’estil de vida que durant les últimes dècades s’està imposant a la nostra societat afavoreix el desequilibri del balanç energètic i en conseqüència l’aparició de la síndrome metabòlica, amb les implicacions que suposa no només en salut pública sinó també a nivell socioeconòmic. Malgrat que existeixen treballs que evidencien afectes beneficiosos sobre paràmetres de la síndrome metabòlica atribuïts al consum de soja i te verd, les vies moleculars d’actuació dels seus principals biocompostos no han estat encara totalment caracteritzades. En aquesta tesi s’ha descrit que les vies d’actuació i els mecanismes en els que participen les isoflavones genisteïna, daidzeïna i el seu metabòlit equol, contribuirien a una millora de la hiperglucèmia, la hiperlipidèmia, la inflamació i l’esteatosi hepàtica, importants components de la fisiopatologia de la síndrome metabòlica en humans. Per altra banda, s’ha demostrat que la principal catequina del te verd, el gal•lat d’epigal•locatequina, actua mitjançant la seva autooxidació, com a senyalitzador cel•lular, induint un desacoblament mitocondrial compensat per un augment de l’activació d’AMPK. Aquestes troballes contribueixen a una descripció dels mecanismes d’acció que podrien explicar els efectes beneficiosos sobre les alteracions del metabolisme energètic associats al consum de soja i te verd. / El estilo de vida que durante las últimas décadas se está imponiendo en nuestra sociedad favorece el desequilibrio del balance energético y con ello el desarrollo del síndrome metabólico, cuyas patologías asociadas son la principal causa de muerte en los países desarrollados. Aunque existen trabajos que evidencian efectos beneficiosos sobre parámetros del síndrome metabólico atribuidos al consumo de soja y té verde, las vías moleculares de actuación de sus principales biocompuestos no han sido aún caracterizadas. En esta tesis se ha descrito no sólo las vías sino también los mecanismos mediados por las isoflavonas genisteína, daidzeína y su metabolito equol, en modelos in vitro insulinorresistentes de los principales tejidos diana de la acción insulínica. Por su parte, se ha demostrado que la principal catequina del té verde, el galato de epigalocatequina, actúa mediante su autooxidación, como señalizador celular, induciendo un desacoplamiento mitocondrial, que se compensa por un incremento de la activación de AMPK. Estos hallazgos contribuyen a la descripción más de los mecanismos de acción que podrían explicar los efectos beneficiosos sobre los desajustes del metabolismo energético asociados al consumo de soja y té verde / Changes in Life style during the last decades in our society has lead to a shift of the energy balance directly associated to the development of metabolic syndrome that nowadays are the main cause of death in developed countries. Although beneficial effects of soy and green tea ingestion have been described previously, the molecular mechanisms of their main biocompounds have not been completely characterized yet. The aim of this thesis is to provide knowledge to help dilucidate them. In this context, the mechanism of action of the isoflavones genistein, daidzein and its metabolite equol have been described with potential interest to improve hyperglycemia, hyperlipidemia, inflammation and hepatic steatosis. On the other hand, it has been demonstrated that the main catechin of green tea, epigallocatequin gallate, through its autooxidation products, modifies cell signalling, leading to a mitochondrial uncoupling compensated by activation of AMPK. In conclusion, these findings offer a more detailed description of the action mechanisms that justify part of the beneficial effects of soy and green tea ingestion on alterations of energy metabolism.

Background: Lung dysfunction constitutes a severe complication after major cardiac surgery with cardiopulmonary bypass (CPB), substantially contributing to postoperative morbidity and mortality. The current possibilities of preventive and therapeutic interventions, however, remain insufficient. We, therefore, investigated the effects of intraoperative application of the antioxidant and anti-inflammatory green tea polyphenol epigallocatechin-3-gallate (EGCG) on CPB-associated lung injury. Materials and methods: Thirty piglets (8 - 15 kg) were divided into four groups: sham-operated and saline-treated control group (n = 7); sham-operated and EGCG-treated control group (EGCG-control group; n = 7); CPB group (n = 10); and CPB + EGCG group (n = 6). The CPB groups underwent 120 min of CPB followed by 90 min of recovery time. In the CPB + EGCG group, EGCG (10 mg/kg body weight) was administered intravenously before and after CPB. Hemodynamic monitoring, blood gas analysis, hematoxylin-eosin staining, and immunohistochemistry of lung tissue were performed. Results: Histologic examination revealed thickening of the alveolar wall and enhanced alveolar neutrophil infiltration in the CPB group (P < 0.05) compared with those in the control group, which was prevented by EGCG (P < 0.05). In the CPB group, higher formation of poly(ADP-ribose) and nuclear translocation of apoptosis-inducing factor were detected in comparison with those in the control group (P < 0.001), which were both reduced in the CPB + EGCG group (P < 0.001). Compared with the control group, the EGCG-control group showed thickening of the alveolar wall and increased neutrophil infiltration (P < 0.05). Conclusions: CPB leads to lung edema, pulmonary neutrophil infiltration, and presumably initiation of poly(ADP-ribose) polymerase-dependent cell death signaling in the lung. EGCG appears to attenuate CPB-associated lung injury, suggesting that this may provide a novel pharmacologic approach.

Indiana University-Purdue University Indianapolis (IUPUI) / Down syndrome (DS) is caused by three copies of human chromosome 21 (Hsa21) and results in an array of phenotypes including intellectual disability. Ts65Dn mice, the most extensively studied DS model, have three copies of ~50% of the genes on Hsa21 and display many phenotypes associated with DS, including cognitive deficits. DYRK1A is found in three copies in humans with Trisomy 21 and in Ts65Dn mice, and is involved in a number of critical pathways including CNS development and osteoclastogenesis. Epigallocatechin-3-gallate (EGCG), the main polyphenol in green tea, inhibits Dyrk1a activity. We have shown that a three-week EGCG treatment (~10mg/kg/day) during adolescence normalizes skeletal abnormalities in Ts65Dn mice, yet the same dose did not rescue deficits in the Morris water maze spatial learning task (MWM) or novel object recognition (NOR). Others have reported that An EGCG dose of 2-3 mg per day (90mg/ml) improved hippocampal-dependent task deficits in Ts65Dn mice. The current study investigated deficits in a radial arm maze pattern separation task in Ts65Dn mice. Pattern separation requires differentiation between similar memories acquired during learning episodes; distinguishing between these similar memories is thought to depend on distinctive encoding in the hippocampus. Pattern separation has been linked to functional activity of newly generated granule cells in the dentate gyrus. Recent studies in Ts65Dn mice have reported significant reductions in adult hippocampal neurogenesis, and after EGCG treatment, enhanced hippocampal neurogenesis. Thus, it was hypothesized that Ts65Dn mice would be impaired in the pattern separation task, and that EGCG would alleviate the pattern separation deficits seen in trisomic mice, in association with increased adult hippocampal neurogenesis. At weaning, Ts65Dn mice and euploid littermates were randomly assigned to the water control, or EGCG [0.4 mg/mL], with both treatments yielding average daily intakes of ~50 mg/kg/day. Beginning on postnatal day 75, all mice were trained on a radial arm maze-delayed non-matching-to-place pattern separation task. Euploid mice performed significantly better over training than Ts65Dn mice, including better performance at each of the three separations. EGCG did not significantly alleviate the pattern separation deficits in Ts65Dn mice. After the behavioral testing commenced, animals were given ad libitum food access for five days, received a 100mg/kg injection of BrdU, and were perfused two hours later. Coronal sections through the dorsal hippocampus were processed for BrdU labeling, and cells were manually counted throughout the subgranular zone of the dentate gyrus. The euploid controls had significantly more BrdU labeled cells than Ts65Dn mice, however, EGCG does not appear to increase proliferation of the hippocampal neuroprogenitor cells. This is the first report of deficits in Ts65Dn mice on a pattern separation task. To the extent that pattern separation depends on the functional involvement of newly generated neurons in an adult dentate gyrus, this approach in Ts65Dn mice may help identify more targeted pharmacotherapies for cognitive deficits in individuals with DS.