Tocilizumab and Dexamethasone Reduce TNF-α and IL-33 and Oxidative Stress in Kidney Tissue in Oleic Acid-Induced ARDS Model.

The most common extrapulmonary organ injury in cases of acute respiratory distress syndrome (ARDS) is acute kidney injury (AKI). This study was designed to investigate the effects of tocilizumab and dexamethasone on antioxidant and proinflammatory cytokines in acute renal injury in rats with an oleic acid-induced ARDS model. Six groups of rats were included in the research: (i) the CN group, (ii) OA group, (iii) OA + TCZ-2 group, (iv) OA + TCZ-4 group, (v) OA + DEX-0.1 group, and (vi) OA + DEX-10 group. The lipid peroxidation levels and superoxide dismutase activities in the kidneys were statistically decreased in the OA + TCZ-4 group. Glutathione levels were increased in the kidneys of rats in the OA group. Catalase activity increased in the OA + TCZ-4 and OA + DEX-10 groups. Tumor necrosis factor-alpha (TNF-α) and interleukin-33 (IL-33) expression levels decreased in the OA + TCZ-4 group. Histopathological findings such as atrophy/hypertrophy in the glomerulus, degeneration and necrosis in the tubular epithelium, hyaline debris in the tubule lumen, and capillary congestion were less prevalent in the OA + TCZ-4 group. Renal SEM imaging revealed severe podocyte surface deterioration and structural damage to tubules in the OA, OA + TCZ-2 and OA + DEX-10 groups. Tocilizumab treatment at a dose of 4 mg/kg appeared to be more effective in certain evaluated parameters compared to other treatments in improving renal glomerular and tubular damage, expression levels of proinflammatory cytokines (TNF-α and IL-33), and antioxidant parameters in cases of oleic acid-induced ARDS.