Mechanism of Dexmedetomidine on Brain Injury in Mice with Sepsis

Abstract

In order to explore the mechanism of dexmedetomidine on brain damage in sepsis, mice were used to detect the staining of cells with hematoxylin-eosin and terminal-deoxynucleotidyl transferase mediated nick end labeling, the content of Evans blue in the brain, and the expression of TNF-α, IL-1β, malonaldehyde, reactive oxygen species, Bcl-2, Bax, cleaved caspase-3 were explored to understand possible mechanism of dexmedetomidine brain protection. The results showed that firstly, dexmedetomidine could attenuate the abnormal morphological changes of neurons in the brain and neuronal apoptosis, secondly, dexmedetomidine could attenuate the expression of TNF-α, IL-1β, MDA, ROS, Bcl-2, Bax, cleaved caspase-3 and iNOS. In summary, the cerebral protection mechanism of dexmedetomidine in septic mice might be connected with reducing the blood brain barrier destruction, reducing brain inflammation and oxidative stress levels, as well as inhibition of apoptosis by altering the expression of Bax, Bcl-2, and cleaved caspase-3. Despite some shortcomings in this investigation, these results still provide clear guidance for future research.