Sepsis-associated encephalopathy is a common
brain diseases, presenting severe diffuse brain dysfunction. The umbilical cord mesenchymal stem cells have been reported to have protective role for treating diseases, while its role in
sepsis-associated encephalopathy remained elusive. This brief report investigated the
therapeutic effect of umbilical cord mesenchymal stem cells on
sepsis-associated encephalopathy in mice model and uncovering the underlying mechanism. The
sepsis-associated encephalopathy mice were injected with 3 mg/kg
lipopolysaccharide. An
enzyme-linked
immunosorbent assay was carried out to determine the production of inflammatory
cytokines. Morris water maze test was used to evaluate mice's neurological dysfunction. Cell apoptosis and tissue injury of the cerebral cortex were assessed using
terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and HE staining.
Evans Blue leakage detection was used to examine the blood-brain barrier integrity. The
protein levels were determined using Western blot. Results showed that the productions of inflammatory
cytokines including
interleukin 6 (IL-6), interleukin-1β (IL-1β),
tumor necrosis factor α (TNF-α), and high mobility group box
protein 1 (
HMGB1) and activated NF-κB were increased in
sepsis-associated encephalopathy mice, which were decreased by umbilical cord mesenchymal stem cells treatment. Besides, umbilical cord mesenchymal stem cells inhibited
lipopolysaccharide-induced cell apoptosis and neuron injury of the cerebral cortex in
sepsis-associated encephalopathy mice. Moreover,
cognitive dysfunction was observed in
sepsis-associated encephalopathy mice, which was alleviated by umbilical cord mesenchymal stem cells. Furthermore, umbilical cord mesenchymal stem cells activated PI3K/AKT signaling pathway. In conclusion, umbilical cord mesenchymal stem cells alleviated
inflammation, cell apoptosis and neuron injury of the cerebral cortex, and
cognitive dysfunction in
sepsis-associated encephalopathy animal model in a PI3K/AKT dependent pathway, making them to be a promising therapeutic strategy for treating
sepsis-associated encephalopathy.