The effect of dexmedetomidine on inflammatory reaction and expression of related cytokines in lung tissues of septic mice
LU Guangtao1, LIN Xuezheng2, YAO Zhangquan2, WANG Junlu1
1.Department of Anesthesiology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China; 2.Department of Anesthesiology, Taizhou Central Hospital, Taizhou 318000, China
LU Guangtao,LIN Xuezheng,YAO Zhangquan, et al. The effect of dexmedetomidine on inflammatory reaction and expression of related cytokines in lung tissues of septic mice[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2019, 49(8): 589-593.
Abstract：Objective: To explore the effect of dexmedetomidine (DEX) on inflammatory reaction and expression of related factors in lung tissues of septic mice stimulated with lipopolysaccharide (LPS). Methods: Male adult C57BL/6 mice were randomly divided into four groups: Control group (group C), Sepsis group (group S), DEX group (group MD) and High dose DEX group (group HD). Group MD and HD were respectively injected DEX solution 25 and 50 μg/kg through tail vein 30 min before modeling, while group C and S were injected equal amount of physiological saline. Septic mice model were then induced by tail vein injection of LPS. Six hours after LPS injection, the protein level of inflammatory cytokines in serum of mice were measured by ELISA kits; Western blot was performed to detect the activity of NF-κB (p65 and IκBα) and AKT. Lung tissues were collected to detect the wet/dry weight ratio (W/D), total lung water content (TLW) and degree of lung tissue injury. Septic model were establised in the same way, mice were monitored every 24 hours and recorded the survival rate for 7 days. Results: Compared with group C, there was a significant elevation in the protein level of TNF-α, CXCL1, CXCL5 and CCL20 (P<0.01) in group S, while DEX can inhibit the level of above-mentioned cytokines. Compared with group S, the pretreatment with DEX can significantly reduce the phosphorylation level of p65, IκBα and AKT (P<0.05), W/D ratio and TLW (P<0.05), and the degree of lung tissue injury. In addition, survival studies indicated that DEX significantly prolonged the survival time of septic mice (P<0.05). Conclusion: Pretreatment with DEX may protect lung tissues in septic mice by reducing the expression of AKT and NF-κB, and inhibiting the expression of inflammatory cytokines.
