Background: Skin wounds can occur for many reasons, including UV radiation, mechanical burns, trauma, and chronic inflammation caused by metabolic factors. In Mongolia, as of 2022, household burns were the top 5 causes of injuries, the leading cause of injuries in children aged 0-5, and accounted for 18.4% of all illnesses in children aged 0-5. Skin burns and wounds take a long time to heal, which causes emotional, aesthetic, and economic stress for doctors. Developing in novative, effective, and low-side effects therapeutic products to improve wound healing is of great clinical and economic importance. The lack of research on the effects of bacterial metabolites and aloe vera (Aloe barbadensis Miller) on burn wounds was the basis for our research. Aim: To determine the effects of a mixture of bacterial metabolites and aloe vera on burn wounds in experimental animals. Materials and Methods: Eight-week-old BALB/c mice were divided into three groups: control group, bacterial metabo lite group, and aloe vera group. The mice were anesthetized, and the dorsal hair was shaved over a 2×2 cm area using an electric clipper. A second-degree burn wound model was created by exposing the shaved dorsal skin to hot air at 200°C for 10 seconds. A total of 100 μL of a bacterial metabolite suspension mixed with aloe vera at a 1:1 ratio was applied evenly to the center of the wound. Wound images were captured daily, and wound areas were measured using ImageJ software. Healing was evaluated on days 7, 14, and 21 of treatment and compared with the control group. The initial wound size was defined as 100%, and wound closure percentages were calculated accordingly. Burn skin tissues from both experimen tal and control groups were subjected to immunofluorescence staining for the vascular marker α-SMA (Thermo Fisher Scientific). Statistical analysis: The differences between the control and experimental groups were analyzed using an independent t-test using GraphPad Prism 10 software, and the mean, standard deviation, and statistical correlation were calculated. Results: The effect of the mixture of bacterial metabolites and aloe vera (Aloe barbadensis Miller) on the healing of burn wounds in experimental mice was compared with the control group. The wound size at 7 days was 82.1% in the control group and 83.7% in the experimental group (p<0.197), at 14 days was 62.6% in the control group and 58.1% in the exper imental group (p<0.0001), at 21 days was 50.7% in the control group and 32.7% in the experimental group (p<0.0001). No statistically significant difference in wound healing was observed between the groups at day 7; however, significant differences were observed at days 14 and 21. Immunofluorescence analysis revealed uniform expression of α-SMA-pos itive cells in the experimental group at 7, 14, and 21 days of treatment, whereas α-SMA expression was not detected in the control group. Conclusion The combination of bacterial metabolites and aloe vera promotes wound healing in experimental mouse burn wounds.

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 minutes. 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.