Daidzein is a phytoestrogen isoflavone found in soybeans and other legumes. The chemical composition of daidzein is analogous to mammalian estrogens, and it could be useful with a dual‐directional purpose by substituting/hindering with estrogen and estrogen receptor (ER) complex. Hence, daidzein puts forth shielding effects against a great number of diseases, especially those associated with the control of estrogen, such as breast cancer, diabetes, osteoporosis, and cardiovascular disease. However, daidzein also has other ER‐independent biological activities, such as oxidative damage reduction acting as an antioxidant, immune regulator as an anti‐inflammatory agent, and apoptosis regulation, directly linked to its potential anticancer effects. In this sense, the present review is aimed at providing a deepen analysis of daidzein pharmacodynamics and its implications in human health, from its best‐known effects alleviating postmenopausal symptoms to its potential anticancer and antiaging properties.

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a tangle-shaped accumulation of beta-amyloid peptide fragments and Tau protein in brain neurons. The pathophysiological mechanism involves the presence of Aβ-amyloid peptide, Tau protein, oxidative stress, and an exacerbated neuro-inflammatory response. This review aims to offer an updated compendium of the most recent and promising advances in AD treatment through the administration of phytochemicals. The literature survey was carried out by electronic search in the following specialized databases PubMed/Medline, Embase, TRIP database, Google Scholar, Wiley, and Web of Science regarding published works that included molecular mechanisms and signaling pathways targeted by phytochemicals in various experimental models of Alzheimer’s disease in vitro and in vivo. The results of the studies showed that the use of phytochemicals against AD has gained relevance due to their antioxidant, anti-neuroinflammatory, anti-amyloid, and anti-hyperphosphorylation properties of Tau protein. Some bioactive compounds from plants have been shown to have the ability to prevent and stop the progression of Alzheimer’s.

Several biological activities have been described for polyphenolic compounds, including a modulator effect on the immune system. The effects of these biologically active compounds on the immune system are associated to processes as differentiation and activation of immune cells. Among the mechanisms associated to immune regulation are epigenetic modifications as DNA methylation of regulatory sequences, histone modifications and posttranscriptional repression by microRNAs that influences the gene expression of key players involved in the immune response. Considering that polyphenols are able to regulate the immune function and has been also demonstrated an effect on epigenetic mechanisms, it is possible to hypothesize that there exists a mediator role of epigenetic mechanisms in the modulation of the immune response by polyphenols.

Dental caries is multifactorial disease and an important health problem worldwide. Streptococcus mutans is considered as a major cariogenic agent in oral cavity. This bacteria can synthetize soluble and insoluble glucans from sucrose by glucosyltransferases enzymes and generate stable biofilm on the tooth surface. Biological properties of Chilean propolis have been described and it includes antimicrobial, antifungal, and antibiofilm activities. The main goal of this study was to quantify the concentrations of main flavonoids presents in Chilean propolis and compare some biological properties such as antimicrobial and antibiofilm activity of individual compounds and the mixture of this compounds, against S. mutans cultures. Chilean propolis was studied and some polyphenols present in this extract were quantified by HPLC-DAD using commercial standards of apigenin, quercetin, pinocembrin, and caffeic acid phenethyl ester (CAPE). MIC for antimicrobial activity was determined by serial dilution method and biofilm thickness on S. mutans was quantified by confocal microscopy. Pinocembrin, apigenin, quercetin, and caffeic acid phenethyl ester (CAPE) are the most abundant compounds in Chilean propolis. These polyphenols have strong antimicrobial and antibiofilm potential at low concentrations. However, pinocembrin and apigenin have a greater contribution to this action. The effect of polyphenols on S. mutans is produced by a combination of mechanisms to decrease bacterial growth and affect biofilm proliferation due to changes in their architecture.

Major depressive disorder (MDD) is a chronic disease whose neurological basis and pathophysiology remain poorly understood. Initially, it was proposed that genetic variations were responsible for the development of this disease. Nevertheless, several studies within the last decade have provided evidence suggesting that environmental factors play an important role in MDD pathophysiology. Alterations in epigenetics mechanism, such as DNA methylation, histone modification and microRNA expression could favor MDD advance in response to stressful experiences and environmental factors. The aim of this review is to describe genetic alterations, and particularly altered epigenetic mechanisms, that could be determinants for MDD progress, and how these alterations may arise as useful screening, diagnosis and treatment monitoring biomarkers of depressive disorders.

Cisplatin (CDDP) is the drug of choice against different types of cancer. However, tumor cells can acquire resistance to the damage caused by cisplatin, generating genetic and epigenetic changes that lead to the generation of resistance and the activation of intrinsic resistance mechanisms in cancer cells. Among them, we can find mutations, alternative splicing, epigenetic-driven expression changes, and even post-translational modifications of proteins. However, the molecular mechanisms by which CDDP resistance develops are not clear but are believed to be multi-factorial. This article highlights a description of cisplatin, which includes action mechanism, resistance, and epigenetic factors involved in cisplatin resistance.