Purpose: To investigate the mechanisms through which dexmedetomidine (DEX) could improve the renal injury in lipopolysaccharide (LPS)-induced acute kidney injury (AKI) and examine how TNF-α or DEX might affect mitochondrial function and renal injury.
Methods: In vivo experiments involved 24 rats randomly allocated to a sham group, an LPS group, and an LPS + DEX group. Serum creatinine, lactate, TNF-α, IL-1β, and IL-6 concentrations, as well as urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, were measured 0, 3, and 6 h after the start of the experiments.
The mechanisms by which landiolol, an ultra-short-acting, selective β-1 blocker, could improve septic acute kidney injury and how inflammation might affect mitochondrial function and cause the renal injury were examined. Male Wistar rats (250 g-300 g) were randomly allocated to three groups: a sham control group (n = 8); a lipopolysaccharide (LPS) group (n = 8); and an LPS + landiolol group (n = 8). LPS was administered intravenously at the start of the experiments; the LPS + landiolol group rats received LPS and continuous intravenous landiolol.
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