Abstract

To investigate the protecting effects of dexamethasone (DXM), baicalin and octreotide on brain injury of rats with severe acute pancreatitis (SAP) and explore their underlying mechanism. This experiment was divided into two different parts: (1) In the first part, 90 SAP rats were randomly divided into a model control group and a DXM treated group (n=45, respectively). (2) In the second part, 135 SAP rats were randomly divided into a model control group, a baicalin treated group and an octreotide treated group (n=45, respectively). In two different experiments, the same number of normal rats were considered as the sham-operated group (n=45, respectively). At 3, 6 and 12h after operation, the pathological changes in the brain were observed. The expression levels of nuclear factor-κB (NF-κB), Bax and Bcl-2 proteins were detected and apoptosis indexes were calculated, using brain tissue microarray section. (1) First part: The expression levels of Bax and Bcl-2 were significantly higher in the DXM treated group than those in the model control group at different time points, while the content of NF-κB protein and pathological changes were significantly lower in the treated group than those in the model control group (P<0.05, P<0.01 or P<0.001). But the apoptotic indexes of brain tissue were not significantly different at different time points (P>0.05). (2) Second part: At all time points after operation, the expression levels of NF-κB in the brain of treated groups were, to varying degrees, significantly lower than those in the model control group while the expression levels of Bcl-2 protein in baicalin and octreotide group were significantly higher than those in model control group (P<0.01, P<0.01 and P<0.05, respectively). At 12h after operation, the expression level of Bax protein in baicalin treated group was significantly higher than those in model control group and octreotide treated group (P<0.05 and P<0.01, respectively). Dexamethasone, baicalin and octreotide can exert protective effects against brain injury in SAP rats mainly through inhibiting the expression of NF-κB protein.

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