Acute inflammation is essential for defending the body against pathogens; however, when inflammation becomes chronic, it is harmful to the body and is part of the pathophysiology of various diseases such as Diabetes Mellitus type 2 (DM2) and Cardiovascular Disease (CVD) among others. In chronic inflammation macrophages play an important role, mainly through the secretion of proinflammatory cytokines such as Tumor necrosis factor (TNF)-α and Interleukin (IL)-1β, explained in part by activation of the Toll-like receptor 4 (TLR4), a signaling pathway which culminates in the activation of Nuclear factor (NF)-κB, an important transcription factor in the expression of these proinflammatory genes. On the other hand, the benefits on health of a diet rich in fruit and vegetables are well described. In this work, the effects of aqueous extract of tomato and ferulic acid on the expression of proinflammatory cytokines in LPS activated monocyte-derived THP-1 macrophages were investigated. In addition, using Western blot, we investigated whether the inhibition was due to the interference on activation of NF-κB. We found that both the tomato extract and ferulic acid presented inhibitory activity on the expression of TNF-α and IL-1β cytokine by inhibiting the activation of NF-κB. The current results suggest that tomatoes and ferulic acid may contribute to prevention of chronic inflammatory diseases.

Frailty and cardiovascular diseases are increasingly prevalent in aging populations, sharing common pathological mechanisms, such as oxidative stress. The evidence shows that these factors predispose frail individuals to cardiovascular diseases but also increase the risk of thrombosis. Considering this background, this review aims to explore advances regarding the relationship between oxidative stress, platelet alterations, and cardiovascular diseases in frailty, examining the role of reactive oxygen species overproduction in platelet activation and thrombosis. The current evidence shows a bidirectional relationship between frailty and cardiovascular diseases, emphasizing how frailty not only predisposes individuals to cardiovascular diseases but also accelerates disease progression through oxidative damage and increased platelet function. Thus, oxidative stress is the central axis in the increase in platelet activation and secretion and the inadequate response to acetylsalicylic acid observed in frail people by mitochondrial mechanisms. Also, key biomarkers of oxidative stress, such as isoprostanes and derivate reactive oxygen metabolites, can be optimal predictors of cardiovascular risk and potential targets for therapeutic intervention. The potential of antioxidant therapies in mitigating oxidative stress and improving cardiovascular clinical outcomes such as platelet function is promising in frailty, although further research is necessary to establish the efficacy of these therapies. Understanding these mechanisms could prove essential in improving the health and quality of life of an aging population faced with the dual burden of frailty and cardiovascular diseases.

Introducción. El envejecimiento acelerado de la población aumenta el riesgo de aparición de complicaciones geriátricas, como el deterioro cognitivo. Este deterioro se ha relacionado con el síndrome de fragilidad y la polifarmacia en cohortes europeas; sin embargo, su relación no se ha aclarado completamente en las personas mayores latinoamericanas. El objetivo de este estudio fue evaluar la relación entre el deterioro cognitivo, la polifarmacia y el síndrome de fragilidad en adultos mayores chilenos. Metodología. El estudio se diseñó como un estudio transversal. El total de participantes fue de 1205 adultos mayores, de 65 años o más. La presencia de fragilidad se determinó según los criterios de Fried. El estado de polifarmacia se evaluó mediante un cuestionario validado realizado por un entrevistador capacitado. El estado cognitivo se determinó mediante el Mini-Mental. Resultados. La prevalencia del deterioro cognitivo en el estudio transversal fue del 19%. Los adultos mayores con deterioro cognitivo tenían una puntuación de fragilidad más alta (2.39 ± 1.45, p < 0.001), una mayor prevalencia de fragilidad y una mayor prevalencia de polifarmacia (45.6%, p = 0.0016) en comparación con los adultos mayores con cognición normal. Los criterios de fragilidad pérdida de peso (OR: 1.88, IC = 1.22-2.90, p = 0.004), agotamiento (OR: 2.66, IC = 1.89-3.76, p<0.001), lentitud (OR: 2.10, p<0.001) y baja actividad física (OR: 1.59, p=0.009) se asociaron con deterioro cognitivo; sin embargo, los criterios de debilidad no presentaron una asociación significativa (OR: 1.29, IC=0.94-1,80, p=0.119). Discusión. El deterioro cognitivo estaba presente en el 19% de las personas mayores y estaba relacionado con el envejecimiento, el bajo nivel educativo, el hecho de vivir solo, la fragilidad y la polifarmacia. Conclusiones. Las estrategias de intervención dirigidas a la fragilidad y al consumo excesivo de medicamentos pueden ser un enfoque prometedor para prevenir el deterioro cognitivo.