As a life-threatening multiple organ dysfunction attributable to maladjusted host immune responses to
infection,
sepsis is usually the common pathway to serious prognosis and death for numerous
infectious diseases all over the world.
Sepsis-associated encephalopathy (SAE) is frequently complicated by septic conditions, and is one of the most important reasons for increased mortality and poor outcomes in septic patients which is still an urgent clinical problem need to be solved. In this research, a conspicuously discovery of treatment-related translational use for
berberine was elaborated. The results revealed that
berberine treatment significantly restored
cognitive impairment in
sepsis mice. Reduced expression levels of TNF-α, IL-1α, and C1qA were exhibited in the hippocampus of the
berberine treatment group, and attenuated effect of declining neo-neuron, activation of microglia and astrocytes in the hippocampus of mice with
sepsis were also found. Moreover,
berberine inhibits microglia-stressed A1 astrocytes by inhibiting
HMGB1 signaling was revealed, then the molecular mechanism of
HMGB1/RAGE signaling inhibition leads to the better outcome of SAE was elucidated. To summarize, this research indicated that
berberine targets
HMGB1/RAGE signaling to inhibit microglia-stressed A1 astrocyte and neo-neuron decline, which consequently alleviates
sepsis-induced
cognitive impairment. Collectively,
berberine may serve as potential therapeutic drug and
HMGB1/RAGE signaling would be a novel target for medicine development for treating SAE.