Abstract:Objective:To explore the possible mechanism of the protective effect of breviscapine on brain tissue in rats with acute hemorrhagic necrotizing pancreatitis, and to provide theoretical basis for the clinical treatment and prevention of pancreatic encephalopathy.
Methods :A total of 90 male SD rats were randomly divided into three groups with 30 rats for each group: normal control group (C group), acute hemorrhagic necrotizing pancreatitis group (AHNP group) and AHNP treated with breviscapine group(T group).The acute hemorrhagic necrotizing pancreatitis model in rats was induced by retrograde injection of 5％ sodium taurocholate into the pancreatobiliary duct. The brain samples were obtained in each group after the rats were killed at 6，12 and 24 hours respectively after operation. The activity of NF-κB and PKC-α in brain tissue was detected with immunohistochemistry and the expression of PKC-α mRNA in brain tissue was detected with RT-PCR. The level of serum TNF-α was measured by radioimmunoassay (RIA) and the changes of brain water content were measured.
Results:In T group, the activity of PKC-α and NF-κB, the expression of PKC-α mRNA in rat brain tissue, the serum TNF-α level and the changes of brain water contents were decreased significantly compared to the AHNP group(P<0.05).
Conclusions:Breviscapine can reduce inflammatory mediators by suppressing the activity of PKC-α, and then alleviate the acute pancreatitis-associated brain injury.