Halici, Hamza; Un, Harun; Celik, Saffet; Karakoy, Zeynep; Bayraktutan, Zafer; Ozlu, Can; Cadirci, Elif; Halici, Zekai; Atila, Alptug; Mercantepe, Filiz

Bee venom is secreted by a gland in the abdominal cavity of bees. The venom, especially that of honeybees, contains certain enzymes and peptides that, when administered in high doses, are effective against various diseases. Peptides such as melittin and phospholipase A2 can target various cancer cells. In this study, we investigated the antiproliferative effects of administering low-dose bee venom in K-562 chronic myeloid leukaemia cells. Our proteomic study revealed regional variation of the content of bee venom and high levels of melittin, apamin and secapin, as well as phospholipase A2 and hyaluronidase. In addition, eight new, previously unidentified proteins were identified. The effects of bee venom on cell viability and drug–cell interaction were investigated at 24, 48 and 72 h. According to the MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) results, the bee venom decreased K-562 cell viability dose-dependently at all time points. Cell viability decreased 48 and 72 h after bee venom administration but increased in the control group left untreated for 72 h. The inhibition percentages for the highest bee venom concentration (0.4 µM) at 24, 48 and 72 h were 55%, 80% and 92%, respectively. The cell–drug interactions indicated that the cell surfaces, which were smooth and clear before drug application, gradually deteriorated and started to shrink after the application. In conclusion, at increasing doses, bee venom was found to have a strong antiproliferative effect in K-562 chronic myeloid leukaemia cell lines.

Celik, Mine; Koca, Mehmet; Halici, Zekai; Tavaci, Taha; Halici, Hamza; Ozkaraca, Mustafa; Karakoy, Zeynep; Bayraktutan, Zafer

Considering the limited treatment options for acute lung injury (ALI) and pulmonary fibrosis (PF), ozone treatment may be promising as a new immunological agent with its ability to modulate cytokines and interferons. We aimed to investigate the effects of inhaled ozone therapy on both ALI and PF in rat models. A total of 48 albino Wistar male rats were included in the study. Lipopolysaccharide (LPS) was used to induce the ALI model, and bleomycin was used for the PF model. The effects of inhaled ozone (O3) were investigated using the ELISA method. Hematoxylin&eosin staining, Masson’s trichrome staining, and immunohistochemical methods were used for histopathological evaluation. The Interleukin-1 beta (IL-1β), Interleukin-6 (IL-6), Tumor Necrosis Factor-alpha (TNF-α), and Nuclear Factor kappa B subunit p65 (NF-κB p65) levels in the ALI + 0.08 ppm O3, ALI + 0.12 ppm O3, PF + 0.08 ppm O3, and PF + 0.12 ppm O3 groups statistically decreased to the same extent and approached the levels of control animals. It was observed that IL-1β, IL-6, TNF-α, and NF-κB p65 levels in lung tissues were significantly and dose-dependently decreased compared to the untreated PF and ALI groups, respectively. While fibrosis was severe in the PF + 0.08 ppm O3 group, it decreased to more moderate levels in the PF + 0.12 ppm O3 group. The cytokine levels confirmed that inhaled ozone protected the lungs from both ALI and the development of PF.