ABSTRACT
BACKGROUND: Currently offered therapeutics to treat colon cancer (CoCa) are toxic when given at maximum tolerated dose to achieve optimal clinical response. Hence, less toxic therapeutic intervention is needed to treat CoCa. In this study, we investigated the effect of a natural agent, Emodin, on CoCa. METHODS: Cell viability (MTT) assay was used to determine the effect of Emodin on human CoCa and colon epithelial cells. Flow cytometric analysis was used to determine Emodin induced cell death. Antibody microarray and western blot analyses were used to determine Emodin induced molecular changes involved in cell death. Change in mitochondrial membrane potential in response to Emodin was determined by flow cytometric analysis. Expression and localization of Bcl-2 family proteins were assessed by western blot analysis. RESULTS: Emodin decreased viability of CoCa cells and induced apoptosis in a time and dose-dependent manner compared to vehicle-treated control without significantly impacting normal colon epithelial cells. Emodin activated caspases, modulated Bcl-2 family of proteins and reduced mitochondrial membrane potential to induce CoCa cell death. Further, changes in Bcl-2 family protein expression and localization correlated with loss in mitochondrial membrane potential. Signaling (MAPK/JNK, PI3K/AKT, NF-κß and STAT) pathways associated with cell growth, differentiation, and Bcl-2 family expression or function were negatively regulated by Emodin. CONCLUSIONS: Ability of Emodin to impact molecular pathways involved in cell survival and apoptosis highlight the potential of this agent as a new and less toxic alternative for CoCa treatment.
ABSTRACT
This study presents the morphological and chemical modification of the cell structure of aerosolized Escherichia coli treated with a dielectric barrier discharge (DBD). Exposure to DBD results in severe oxidation of the bacteria, leading to the formation of hydroxyl groups and carbonyl groups and a significant reduction in amine functionalities and phosphate groups. Near edge x-ray absorption fine structure (NEXAFS) measurements confirm the presence of additional oxide bonds upon DBD treatment, suggesting oxidation of the outer layer of the cell wall. Electron microscopy images show that the bacteria undergo physical distortion to varying degrees, resulting in deformation of the bacterial structure. The electromagnetic field around the DBD coil causes severe damage to the cell structure, possibly resulting in leakage of vital cellular materials. The oxidation and chemical modification of the bacterial components are evident from the Fourier transform infrared spectroscopy and NEXAFS results. The bacterial reculture experiments confirm inactivation of airborne E. coli upon treating with DBD.
