The use of honey as an internal and external health agent is much older than the history of medicine itself. The earliest recorded medical prescription including honey is from Sumer. Honey was used as a remedy against a variety of illnesses in ancient Egypt, Greece, and Rome. There are frequent references to honey in sacred texts. Honey has a long tradition, not only in Western medicine but also in traditional Chinese medicine and Ayurveda. Honey was not commonly used by medical practitioners after the fall of the Roman Empire. In medieval times honey was not a popular subject of medical texts and very little was written on its use in that period. In the nineteenth century honey was neglected due to the development of modern synthetic medicine. Its comeback has, however, been observable as early as the beginnings of the twentieth century, and honey has been used again as a remedy for a variety of health problems and an excellent wound healer.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in cancer cells without toxicity to normal cells. TRAIL binds to death receptors, TRAIL-R1 (DR4) and TRAIL-R2 (DR5) expressed on cancer cell surface and activates apoptotic pathways. Endogenous TRAIL plays an important role in immune surveillance and defense against cancer cells. However, as more tumor cells are reported to be resistant to TRAIL mediated death, it is important to search for and develop new strategies to overcome this resistance. Chalcones can sensitize cancer cells to TRAIL-induced apoptosis. We examined the cytotoxic and apoptotic effects of TRAIL in combination with four chalcones: chalcone, isobavachalcone, licochalcone A and xanthohumol on HeLa cancer cells. The cytotoxicity was measured by MTT and LDH assays. The apoptosis was detected using annexin V-FITC staining by flow cytometry and fluorescence microscopy. Death receptor expression was analyzed using flow cytometry. The decreased expression of death receptors in cancer cells may be the cause of TRAIL-resistance. Chalcones enhance TRAIL-induced apoptosis in HeLa cells through increased expression of TRAIL-R2. Our study has indicated that chalcones augment the antitumor activity of TRAIL and confirm their cancer chemopreventive properties.

TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) is an endogenous ligand, which plays role in immune surveillance and anti-tumor immunity. It has ability to selectively kill tumor cells showing no toxicity to normal cells. We tested the apoptotic and cytotoxic activities of xanthohumol, a prenylated chalcone found in Humulus lupulus on androgen-sensitive human prostate adenocarcinoma cells (LNCaP) in combination with TRAIL. Cytotoxicity was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide tetrazolium reduction assay (MTT) and lactate dehydrogenase assay (LDH). The expression of death receptors (DR4/TRAIL-R1 and DR5/TRAIL-R2) and apoptosis were detected using flow cytometry. We examined mitochondrial membrane potential (ΔΨm) by DePsipher reagent using fluorescence microscopy. The intracellular expression of proteins was evaluated by Western blotting. Our study showed that xanthohumol enhanced cytotoxic and apoptotic effects of TRAIL. The tested compounds activated caspases-3, -8, -9, Bid, and increased the expression of Bax. They also decreased expression of Bcl-xL and decreased mitochondrial membrane potential, while the expression of death receptors was not changed. The findings suggest that xanthohumol is a compound of potential use in chemoprevention of prostate cancer due to its sensitization of cancer cells to TRAIL-mediated apoptosis.

Propolis is one of the most used natural supplements, and its composition and biologically active properties vary from region to region. In this study, conducted as a case study, the phenolic profiles, volatile compounds and antioxidant activities of propolis samples from two different regions were compared. The phenolic compositions of the ethanol extracts were examined as total phenolic content (TPC) and total flavonoid content (TFC) and phenolic compositions. Phenolic compounds were analyzed using high-performance liquid chromatography-photo diode array (HPLC-PDA) according to the method using 25 phenolic standards. Antioxidant capacities were assessed using ferric reducing/ antioxidant power (FRAP) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) assays. Volatile compounds were analyzed using headspace solid-phase microextraction gas chromatography-mass spectrometry (HS-SPME-GC-MS). The average TPC and TFC values in the Polish and Turkish pooled propolis samples were determined as 187.16 ± 3.03 mg GAE/g and 44.69 ± 1.02 mg QUE/g and 198.09 ± 2.50 mg GAE/g and TFC 54.26 ± 0.70 mg QUE/g, respectively. While caffeic acid phenethyl ester (CAPE), myricetin, luteolin and hesperidin were high in the Turkish pooled propolis sample, p-coumaric acid, OH-benzoic acid, pinocembrin and apigenin were found high in the Polish pooled propolis sample. Approximately 133 volatile compounds were identified across both samples, with the Turkish pooled propolis sample demonstrating a notably higher presence of compounds such as verbenone, carveol, carvone, α-pinene, limonene, and β-eudesmol. The Turkish pooled propolis sample demonstrates a higher antioxidant activity in both methods due to its richer phenolic and volatile composition. In conclusion, the chemical composition and antioxidant properties of propolis are significantly influenced by the flora of its region of origin.

Propolis, owing to its antibacterial and anti-inflammatory properties, acts as a cariostatic agent, capable of preventing the accumulation of dental plaque and inhibiting inflammation. The anti-inflammatory properties of propolis are attributed to caffeic acid phenethyl ester (CAPE), which is present in European propolis. The objective of the conducted study was to assess the anti-inflammatory effects of the Polish ethanolic extract of propolis (EEP) and isolated CAPE on stimulated with LPS and IFN-α, as well as the combination of LPS and IFN-α. The cytotoxicity of the tested compounds was determined using the MTT assay. The concentrations of specific cytokines released by the HGF-1 cell line following treatment with EEP (25–50 µg/mL) or CAPE (25–50 µg/mL) were assessed in the culture supernatant. In the tested concentrations, both CAPE and EEP did not exert cytotoxic effects. Our results demonstrate that CAPE reduces TNF-α and IL-6 in contrast to EEP. Propolis seems effective in stimulating HGF-1 to release IL-6 and IL-8. A statistically significant difference was observed for IL-8 in HGF-1 stimulated by LPS+IFN-α and treated EEP at a concentration of 50 µg/mL (p = 0.021201). Moreover, we observed that CAPE demonstrates a stronger interaction with IL-8 compared to EEP, especially when CAPE was administered at a concentration of 50 µg/mL after LPS + IFN-α stimulation (p = 0.0005). Analysis of the phenolic profile performed by high-performance liquid chromatography allowed identification and quantification in the EEP sample of six phenolic acids, five flavonoids, and one aromatic ester—CAPE. Propolis and its compound—CAPE—exhibit immunomodulatory properties that influence the inflammatory process. Further studies may contribute to explaining the immunomodulatory action of EEP and CAPE and bring comprehensive conclusions.

Colon cancer is one of the leading causes of death in the world. The search for effective and minimally invasive methods of treating colon cancer is the aim of modern medicine. Chalcones and their derivatives have shown an anticancer activity. The aim of the study was to evaluate the effect of methoxy-derivatives of 2'-hydroxychalcones: 2'-hydroxy-3"-methoxychalcone (TJ3), 2'-hydroxy-2"-methoxychalcone (TJ6) and 2'-hydroxy-4"-metoxychalcone (TJ7) at the concentrations of 10 µM and 25 µM on the release of IL-8, MIF, VCAM-1, ICAM-1 by colon cancer SW480 and SW620 cell lines. The cytokines and adhesion molecules were detected using the Bio-Plex Magnetic Luminex Assay and the Bio-Plex Suspension Array System. Our results showed that all tested methoxy-derivatives of 2'-hydroxychalcone compounds significantly reduced ICAM-1 released by SW480 cancer cells. The tested compounds at both concentrations did not significantly affect VCAM-1 released by SW480 and SW620 cancer cell lines. All methoxy-derivatives significantly reduced the concentration of MIF in dose dependent manner on SW480 cells. The TJ3 at the concentration of 25 µM significantly decreased IL-8 secreted by SW480 and SW620 cancer cells. Our results demonstrated that tested methoxy-derivatives of 2'-hydroxychalcones showed modulating effect on colon cancer cells.