• İhsan Karaboğa.
• Department of Emergency and Disaster Management, Tekirdağ Namık Kemal University School of Health, Tekirdağ-Turkey.
• Ulus Travma Acil Cer. 2019 Sep 1; 25 (5): 433-439.

BackgroundPulmonary contusion (PC) is an important life-threatening clinical condition characterized by lung injury and inflammation. Caffeic acid phenethyl ester (CAPE) is a biological agent with potent antioxidant and anti-inflammatory effects. This study aimed to investigate the potential effects of CAPE on tissue damage, nuclear factor kappa-beta (Nf-κβ) activity, inducible nitric oxide synthase (iNOS) synthesis, and pulmonary apoptosis in an experimental PC model.MethodsForty adult Wistar albino rats were used in this study and divided into four groups as follows: control, PC, PC + CAPE, and CAPE. CAPE was administered intraperitoneally for seven days following PC formation (10 µmol/kg, dissolved in dimethyl sulfoxide). Wet/dry weight ratio in lung tissue was determined. The pulmonary tissue was examined using hematoxylin-eosin and Masson's trichrome histochemical staining and also by scanning electron microscopy. Nf-κβ and iNOS activities in the lungs were determined by the indirect immunohistochemical method. Pulmonary apoptosis was detected by the TUNEL method.ResultsIncreased leukocyte infiltration score, pulmonary edema, alveolar damage, and increased Nf-κβ and iNOS activities were determined in the PC group. CAPE administration inhibited Nf-κβ and iNOS activities and pulmonary apoptosis.ConclusionIn this study, the findings showed that CAPE inhibited tissue damage by suppressing inflammatory mediators of Nf-κβ and iNOS activities. Also, CAPE was found to be protective in the lung tissue and could be used as a therapeutic agent.

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