Efeitos da Histidina em Macrófagos tratados com LPS

Abstract

Recent studies suggest that histidine, an essential amino acid, contributes to the modulation of the immune response through its antioxidant and anti-inflammatory capacity in cells such as macrophages. In central nervous system immunity, macrophages known as microglia play an essential protective role in neuroinflammatory conditions such as Parkinson's disease and Alzheimer's disease. One macrophage activator is LPS (Lipopolysaccharide), an endotoxin found in the outer membrane of gram-negative bacteria. Alzheimer's disease (AD) is a neurodegenerative disease characterized by synaptic dysfunction and neuronal death. Based on this premise, this study aimed to explore the immunomodulatory effects of histidine in cell cultures of macrophages activated with LPS and thus identify new therapeutic possibilities to attenuate neuronal inflammation. In this way, the use of histidine could reduce inflammation in microglia, modulating the immune response and even delaying neuronal degeneration associated with neuroinflammatory pathologies. To this end, we used a commercial strain of macrophages cultured in RPMI medium with 10% SFB and kept in a CO2 oven at 37°C. Different concentrations of LPS were tested on these cells to assess cell viability via the MTT assay, in order to standardize the best dosage for subsequent tests. For analysis by Raman spectroscopy, the cells were treated with different concentrations of histidine. Of the results obtained so far, the concentration of 0.001 mg/mL of LPS for macrophage activation stands out, since cell activation was the most effective, without causing damage to the cells. Raman spectroscopy showed that histidine acts positively on the pro-inflammatory response of macrophages. It is preliminarily concluded that the 0.001 mg/mL concentration of LPS is satisfactory for activating macrophages without compromising the cells and that histidine alters the macrophage reading, of the concentrations tested, 1% was the most impactful, but such concentrations are not ideal as a treatment for Alzheimer's disease.