RESUMEN
Numerous antimicrobial drugs have been prescribed to kill or inhibit the growth of microbes such as bacteria, fungi, and viruses. Despite the known therapeutic efficacy of these drugs, inefficient delivery could result in an inadequate therapeutic index and several side effects. In order to overcome this adversity, the present study investigated antibiotic drug loading in zeolitic imidazolate frameworks (ZIFs), in association with ZnO nanoparticles with known antimicrobial properties. In an economic synthesis method, the ZnO surface was first converted to ZIF-8 with 2-methylimidazole as a ligand, resulting in a ZnO@ZIF-8 structure. This system enables the high drug-loading efficiency (46%) of an antimicrobial drug, ciprofloxacin, within the pores of the ZIF-8. This association provides a control of the release of the active moieties, in simulated body-fluid conditions, with a maximum of 67% released in 96 h. The antibacterial activities of ZnO@ZIF-8 and CIP-ZnO@ZIF-8 were tested against the Gram-positive Staphylococcus aureus strain and the Gram-negative Pseudomonas aeruginosa strain, showing good growth inhibition. This result was obtained by combining ZnO@ZIF-8 with ciprofloxacin in a minimal inhibitory concentration (MIC) that was 10 times lower than ZnO@ZIF-8 for S. aureus and 200 times lower for P. aeruginosa, suggesting that CIP-ZnO@ZIF-8 may have potential application in prolonged antimicrobial treatment.
RESUMEN
The liver is primarilyresponsible for energy homeostasis and the regulation of lipid, carbohydrate and protein metabolism. Lipid metabolism consists of distributing lipids to peripheral tissues or ensuring their return to the liver to be reprocessed. Additionally, cellular metabolism isregulated by several molecules in different signaling pathways. Lipid homeostasis in the liver is mainly regulated by AKT, AMPK, SREBP, PPAR, and JNK. The PI3K/AKT/mTOR signaling pathway results in the biosynthesis of macromolecules and regulates lipogenesis and the expression of lipogenic genes. AMPK is an energy sensor that regulates metabolism and is activated when stored ATP is depleted, and it is responsible for the suppression of several key lipogenic factors in the liver related to cholesterol and fatty acid synthesis. SREBPs control lipogenic geneexpressionandcholesterol metabolism and actin the nutritional regulation of fatty acids and triglycerides. The continued activation of SREBPs is associated with cellular stress, inflammation and ultimately steatosis. PPARs are intrinsically important regulators of lipid metabolism. These genes are essential tovarious metabolic processes, especially lipid and glucose homeostasis, and can play a role in cell differentiation. JNK signaling is related to insulin resistance and its activation results in decreased mitochondrial activity and fat accumulation. Therefore, the study of cell signaling pathways related to lipid metabolism and liver function may help to identify abnormalities and develop strategies to manage and regulate metabolic disorders and resulting complications.