Effects of Auraptene on cardiac dysfunction after acute respiratory distress syndrome: An experimental study

Dr. Furkan DINCER, Effects of Auraptene on Cardiac Dysfunction After Acute Respiratory Distress Syndrome: An Experimental Study, Bolu Abant Izzet Baysal University Faculty of Medicine, Department of Pediatrics, Thesis of Graduation, Bolu, 2024 Background: Proinflammatory/anti-inflammatory cytokine and oxidant/anti-oxidant imbalances develop in ARDS, which is one of the most important reasons for hospitalization in pediatric intensive care units. These imbalances and the resulting hypoxemia can affect different organs in the body. Cardiac dysfunction during ARDS is important in terms of increasing mortality rates. Auraptene is a coumarin derivative, and studies have found that aureptene has a wide range of effects. The aim of this study was to test whether aurapten, which has antioxidant, immunomodulatory and anti-inflammatory effects, can be used in the treatment of cardiac dysfunction due to acute lung injury. Materials and Methods: A total of 40 male Wistar rats were divided into 5 groups. Acute lung injury was induced by intratracheal LPS. Serum samples were analyzed for TNF-α, IL-10, TAS, TnT and N-terminal-proBNP levels. Samples from the lung and heart were stained with hematoxylin-eosin stain. Results: TNF-α levels in the LPS+dexamethasone and LPS+Aureptene groups were significantly lower than in the LPS group (40.5±13.8 vs. 87.9±24.6 pg/ml, p<0.001) and (57.6±17.6 vs. 87.9±24.6 pg/ml, p=0.007, respectively). Again, IL-10 levels in LPS+dexamethasone and LPS+Aureptene groups were significantly lower than in LPS group (21.2±6.8 vs. 45.9±18.3 pg/ml, p<0.001 and 29.8±6.7 vs. 45.9±18.3 pg/ml, p=0.029, respectively). In contrast, TAS values in the LPS+dexamethasone group were significantly higher than in the LPS group (8.6±2.7 vs. 4.2±2.1 U/ml, p<0.001). There was a non-significant increase in the LPS+Aureptene group (5.8±1.4 vs. 4.2±2.1 U/ml, p=0.708). BNP values in the LPS+dexamethasone and LPS+Aureptene groups were significantly lower than in the LPS group (0.3±0.1 vs. 0.8±0.4 ng/ml, p=0.011 and 0.4±0.2 vs. 0.8±0.4 ng/ml, p=0.046, respectively). Similarly, TnT values in LPS+dexamethasone and LPS+Aureptene groups were significantly lower than those in LPS group (48.7±13.4 vs. 87.7±26.2 pg/ml, p=0.001 and 62.1±18.7 vs. 87.7±26.2 pg/ml, p=0.045, respectively). Cardiac degeneration scores in the LPS+dexamethasone and LPS+Aureptene groups were significantly lower than in the LPS group (0±0 vs. 1.25±0.46, p<0.001 and 0.28±0.48 vs. 1.25±0.46, p=0.005, respectively). Cardiac disorganization scores in the LPS+dexamethasone and LPS+Aureptene groups were significantly lower than in the LPS group (0.14±0.37 vs. 1.12±0.64, p=0.006 and 0.14±0.37 vs. 1.12±0.64, p=0.006, respectively). Cardiac congestion scores in the LPS+dexamethasone and LPS+Aureptene groups were significantly lower than in the LPS group (1.57±0.53 vs. 2.75±0.46, p=0.003 and 1.42±0.53 vs. 2.75±0.46, p=0.002, respectively). Cardiac inflammation scores in the LPS+Aureptene groups were significantly lower than in the LPS group (0±0 vs. 0.62±0.74, p=0.036). Conclusion: This study suggests that myocardial damage may develop secondary to ARDS. It suggests that Aureptene can be used in the treatment of both ARDS and myocardial damage secondary to this picture with its inflammation suppressing and antioxidant effects. Key words: Auraptene, acute lung injury, cardiac dysfunction, TNF-α, IL-10, TAS, BNP, Troponin T