Objective: To investigate the effect of dexmedetomidine on inflammatory factors and oxidative stress of AKI (acute kidney injury) in septic rats.
Methods: Thirty-two male SD rats were randomly divided into the following 4 groups (8 rats in each group): sham operation group, lipopolysaccharide (LPS) group, dexmedetomidine (DEX) + LPS group, yoghurt group Bing (YOH)+DEX+LPS group; the latter three groups were injected with LPS (5 mg/kg) via tail vein 30 minutes before operation respectively; LPS+DEX group was injected with DEX (10 μg/kg) via tail vein 10 minutes before LPS; In the YOH+DEX+LPS group, YOH (1 mg/kg) was intraperitoneally injected 40 min before LPS, and DEX 10 μg/kg was injected via tail vein 10 min before LPS. After 4 hours, the rats were sacrificed to extract samples to measure the levels of interleukin-1β (IL-1β), superoxide dismutase (SOD) and malondialdehyde (MDA) in plasma and kidney tissue, and observe the pathological changes of kidney tissue.
RESULTS: Compared with the sham operation group, the levels of IL-1β and MDA in plasma and renal tissue in the LPS group were significantly increased, SOD was significantly decreased (P<0.05), and the renal pathological damage was severe; compared with the LPS group, the DEX + LPS group The levels of IL-1β and MDA in plasma and kidney tissue were significantly decreased, SOD was significantly increased (P<0.05), and renal pathological damage was also significantly alleviated; Both increased, SOD decreased (P<0.05), and the renal pathological damage was more obvious.
Conclusion: DEX can reduce the inflammatory response and oxidative stress of sepsis-related renal injury, and this effect may be through α2 receptors.