Abstract

To explore the effect of dexmedetomidine (DEX) on high-mobility group box 1 protein (HMGB1) in the serum and spleen in rats with sepsis and the underlying mechanisms. A total of 100 male Wistar rats were randomly divided into five groups: a control group, a sepsis group, a DEX group, an α-bungarotoxin- tetramethylrhodamine (α-BGT) plus DEX group and an α-BGT group (n=20 in each group). In the control group, same volume of normal saline (NS) was administrated, while lipopolysaccharide (LPS) was injected to the vein to develop a classic sepsis model. At the 48th h after LPS injection, the rats were sacrificed, and the blood and spleen were collected. The content of tumor necrosis factor-α (TNF-α) and HMGB1 in blood serum were detected by enzyme-linked immuno sorbent assay (ELISA), and the HMGB1 in the spleen was examined by Western blot. Among the 5 groups, there were statistical significance in the mortality, the serum level of TNF-α and HMGB1, and the content of secreting type of HMGB1 in spleen (all P<0.05), and the serum level of HMGB1 was positively correlated with the content of secreting type of HMGB1 (r=0.863, P<0.05). DEX exert late anti-inflammatory effects in the serum and spleen in rats with sepsis, which is related to the activation of the cholinergic anti-inflammatory pathway.

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