Objective: To investigate the effect of dexmedetomidine on renal function and tight junction protein expression in septic rats.
Methods: Thirty SD rats were randomly divided into dexmedetomidine treatment group (Dex group), sepsis model group (M group), and normal saline control group (C group), 10 rats in each group. The rats in the Dex group were injected with lipopolysaccharide (LPS) 5 mg/kg intravenously, and then injected with Dex 7 μg/kg, 15 minutes later, the dose was adjusted to 5 μg/kg·h, and the infusion was continued for 30 minutes; the model group was given the same method. Physiological saline was pumped after LPS; group C was always given normal saline by the above method. 24 hours later, the blood was collected to separate the plasma, and the multifunctional biochemical analyzer was used to detect the contents of creatinine (Scr) and blood urea nitrogen (BUN); ELISA to detect the contents of IL-1β and TNF-α; Western blot to detect the tight junction proteins ZO-1 and occludin in kidney tissue expression changes.
Results: Compared with the C group, the damage of the model group was heavier, with a large number of inflammatory cells infiltrating, showing glomerulonephritis, while the Dex group had no obvious inflammatory cells and less abnormal cells. Compared with the model group, the damage was lighten. The detection results of renal function and inflammatory factors showed that compared with group C, the levels of Scr, BUN, IL-1β and TNF-α in plasma of each group were significantly increased (P<0.05), and the expression levels of ZO-1 and occludin proteins were the same. Compared with the model group, all indexes in the Dex group were significantly decreased (P<0.05), and the protein expressions of ZO-1 and occludin were increased (P<0.05).
Conclusion: Dexmedetomidine can improve the renal function of acute kidney injury caused by sepsis, inhibit the inflammatory response, increase the tight junction protein, and have a certain protective effect on the kidney.