Bee products, in particular honey, propolis and bee venom, are of growing scientific interest due to their broad spectrum of antimicrobial activity. In the face of increasing antibiotic resistance and the limitations of conventional therapies, natural bee-derived substances offer a promising alternative or support for the treatment of infections. This paper summarizes the current state of knowledge on the chemical composition, biological properties and antimicrobial activity of key bee products. The main mechanisms of action of honey, propolis and bee venom are presented, and their potential applications in the prevention and treatment of bacterial, viral and fungal infections are discussed. Data on their synergy with conventional drugs and prospects for use in medicine and pharmacology are also included. The available findings suggest that, with appropriate standardization and further preclinical and clinical analyses, bee products could become an effective support for the treatment of infections, especially those caused by pathogens resistant to standard therapies.

Exposure to lead is associated with microglial dysfunction and the development of neuroinflammation. This contributes to accelerated neurodegeneration. Even low doses of this element modulate inflammatory responses and might contribute to central nervous system dysfunction. Extracts from the mushroom Hericium erinaceus (HE) possess well-documented neurotropic properties; however, its potential neuroprotective mechanisms under conditions of environmental neurotoxicity remain poorly defined. In this study, we investigated the effects of HE on inflammatory signaling in a microglia-oriented in vitro model using THP-1-derived macrophages exposed to low levels of lead (3.5 µg/dL). In our study, Pb exposure did not increase tumor necrosis factor (TNF) alpha levels but reduced monocyte chemoattractant protein-1 (MCP-1) secretion and altered cyclooxygenase (COX) expression, indicating immune response modulation rather than inflammatory activation. Under combined Pb and HE exposure, a marked shift in cyclooxygenase expression toward COX-2 at both the gene and protein levels was observed, accompanied by increased PGE₂ production; these effects were dose-dependent. The inflammatory signaling was modulated rather than amplified. Also, TNF alpha levels were elevated after combined treatment, whereas gene expression responses were dose-dependent. MCP-1 secretion was fine-tuned toward control values, consistent with macrophage morphological changes, while IL-6 levels were increased. Overall, these findings indicate that Hericium erinaceus exerts immunomodulatory effects in microglia-like cells under low-level lead exposure, supporting its neuroprotective potential through modulation of neuroinflammatory signaling.

Folate receptor alpha (FRα) plays a key role in folate homeostasis. Folate is involved, among other processes, in nucleotide biosynthesis, and the marked difference between FRα expression in certain cancers and under physiological conditions gives this receptor potential as a cancer biomarker. However, the current state of knowledge points to a specific role for this marker and defines its potential place in cancer diagnosis and treatment. This review aims to critically evaluate the available evidence regarding the clinical utility of FRα. Analysis of the literature indicates that despite differences in expression, the sensitivity and specificity of FRα are insufficient for its use as a standalone diagnostic marker. In contrast, its potential as a prognostic marker is strongly dependent on cancer type. The strongest evidence of clinical utility concerns membranous FRα protein expression assessed by a validated immunohistochemical companion diagnostic assay for selecting patients with platinum-resistant ovarian cancer for mirvetuximab soravtansine treatment. In contrast, the predictive relevance of FRα for other targeted therapeutic strategies remains under investigation. Overall, FRα should be regarded as a clinically actionable biomarker in a defined therapeutic setting and as a promising, but not universally validated, diagnostic, prognostic, and predictive candidate in other oncological applications.

The progesterone receptor (PGR) is involved in processes associated with tumor progression, also in glioblastoma multiforme (GBM). GBM is characterized by regional heterogeneity, with distinct tumor areas differing in their cellular profiles and access to nutrients and oxygen. The aim of this study was to assess the effect of the tumor microenvironment on PGR mRNA and protein expression and to characterize PGR expression in different regions of GBM. To this end, GBM tumor tissues were collected from patients, and an in vitro model was established using the U87 cell line to reproduce hypoxic (H) and nutrient-deficient (ND) conditions. PGR mRNA expression was assessed by real-time PCR, while PGR protein expression was analyzed using ELISA, Western blot, confocal microscopy, and immunohistochemistry. The microenvironmental conditions examined, including H and ND, did not affect PGR protein expression in U87 cells, while H conditions significantly increased PGR mRNA expression. Different GBM regions showed variable levels of PGR protein expression, with the highest expression observed at the peritumoral area. No effect of sex on PGR expression was observed in any of the GBM regions analyzed. Overall, the results indicate regional heterogeneity of PGR expression in GBM.