ABSTRACT
OBJECTIVES: Sustained stress can cause physiological disruption in crucial systems like the endocrine, autonomic, and central nervous system. In general, skin damages are physical stress present in hospitalized patients. Also, these pressure injuries lead to pathophysiological mechanisms involved in the neurobiology of mood disorders. Here, we aimed to investigate the behavioral alterations, oxidative stress, and corticosterone levels in the brain areas of mice submitted to the model of pressure injury (PI). METHODS: The male mice behaviors were assessed in the open field test (OFT), elevated plus maze test (EPM), tail suspension test (TST), and sucrose preference test (SPT). Then, we isolated the prefrontal cortex (PFC), hippocampus (HP), and striatum (ST) by brain dissection. The nonprotein sulfhydryl groups (NP-SH) and malondialdehyde (MDA) were measured in the brain, and also the plasma corticosterone levels were verified. RESULTS: PI model decreased the locomotor activity of animals (p<0.05). Considering the EPM test, the PI group showed a decrease in the open arm activity (p<0.01), and an increase in the closed arm activity (p<0.05). PI group showed an increment in the immobility time (p<0.001), and reduced sucrose consumption (p<0.0001) compared to the control groups. Regarding the oxidative/nitrosative profile, all brain areas from the PI group exhibited a reduction in the NP-SH levels (p<0.0001-p<0.01), and an increase in the MDA level (p<0.001-p<0.01). Moreover, the PI male mice presented increased levels of plasma corticosterone (p<0.05). CONCLUSIONS: Our findings suggest that the PI model induces depressive and anxiety-like behaviors. Furthermore, it induces pathophysiological mechanisms like the neurobiology of depression.
