Background: The study of small-molecule compounds with antitumor activity involves several crucial steps. These include determining their selective effects on cancer cells, understanding the type of cell death they induce, identifying the activated signaling pathways, pinpointing the target molecules, and elucidating the mechanisms of action. Among the plant-derived compounds with anticancer properties, flavonoids are notable for their ease of isolation and their abundance in food. Apigetrin, a representative flavonoid, is a secondary metabolite found in plants, and our previous study indicated that its anticancer selectivity index was 13.1. However, the specific mechanism by which apigetrin inhibits leukemia cell growth remains unclear. Aim: To study of the inhibitory action of apigenin on leukemia cell culture Materials and Methods: In this study, we evaluated the apoptosis of cells using flow cytometry and investigated the in volvement of the caspase pathway through the use of pancaspase inhibitors to explore the effects of apigetrin on leukemia cell growth. Results: After incubating leukemia RAW264.7 cells with 30 μM apigetrin for 24 and 48 hours, we did not detect any apoptosis through Annexin V and PI staining by flow cytometry. We compared the number of viable cells using the MTT assay after 24-hour treatment of apigetrin with or without pretreatment of Z-VAD, a pancaspase inhibitor, for 30 min utes. The results indicated that the pancaspase inhibitor did not reduce the inhibitory effect of apigetrin on the growth of RAW264.7 cells. In contrast, the positive control group, treated with doxorubicin—which induces apoptosis—showed not only significant apoptosis but also a reduction of the pancaspase inhibitor on the cell growth inhibition. Therefore, these data suggested that apigetrin likely has a cytostatic effect or inhibits the cell cycle rather than being cytotoxic. Future research should focus on determining which stage of the cell cycle RAW264.7 cells treated with apigetrin are in, as well as studying the signaling pathways involved in the cell cycle. Conclusions Apigetrin inhibits the proliferation of RAW264.7 leukemia cells in a caspase-independent and non-apoptotic manner.

Background: In recent years, the incidence of liver diseases due to complications of non-alcoholic fatty liver disease (NAFLD) has shown a significant upward trend in Southeast Asian countries. NAFLD is a hepatic disorder characterized by lipid accumulation in the microstructure of the liver in individuals who consume little to no alcohol. It is often associ ated with insulin resistance and is diagnosed when steatosis affects more than 5% of hepatocytes histologically, or when the fat signal intensity on MRI exceeds 5.6%, based on fat-to-water ratio measurements. In Mongolia, histological studies using frozen liver sections with routine and special staining techniques are limited, highlighting the necessity of this study. Aim: To determine and compare the degree of steatosis and fibrosis in frozen liver tissue samples of patients with NAFLD through histological analysis. Materials and Methods: This study was conducted at the the Department of Anatomy, School of Biomedicine and Bio medical Research Institute of MNUMS in collaboration with the Second State Central Hospital. Ethical approval was obtained from the Research Ethics Committee of MNUMS (Protocol No. 2024/3-06). All procedures adhered strictly to laboratory biosafety protocols. Participants were selected among patients undergoing elective laparoscopic cholecystec tomy, from whom informed consent was obtained. Based on inclusion criteria, five participants were grouped as follows: healthy control (n=1), NAFLD without fibrosis (n=2), and NAFLD with fibrosis (n=2). Liver biopsies (approx. 1 cm in size) were obtained intraoperatively, immediately deep-frozen in liquid nitrogen, and prepared for histological evaluation. Results: In patients with NAFLD compared to the healthy liver group, disruption of hepatocyte columnar architecture and mild periportal lymphocytic infiltration were observed. Oil Red O staining revealed 34–66% micro- and macrovesicular steatosis, corresponding to grade 2 steatosis. Masson’s trichrome staining showed no fibrotic changes in perivenular or periportal areas (Ishak grade 0/4) at this stage. However, upon progression to grade 3 steatosis, early-stage fibrosis was observed in both perivenular and periportal regions (Ishak grade 1/4). Further progression to stage 4 fibrosis was char acterized by the development of connective tissue septa, although no significant changes in droplet size were observed. Conclusions 1. Increasing stages of fibrosis are not directly influenced by the severity of hepatic steatosis in NAFLD. 2. Although the degree of steatosis increases, the absence of corresponding fibrotic changes in early stages indicates a complex progression pattern of NAFLD requiring further investigation.