Caffeic Acid Phenethyl Ester Ameliorates Pulmonary Inflammation and Apoptosis Reducing Nf-κβ Activation in Blunt Pulmonary Contusion Model

Abstract

BACKGROUND: Pulmonary 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. METHODS:Forty 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.RESULTS: Increased 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. CONCLUSION:In this study, the findings showed that CAPE inhibited tissue damage by suppressing inflammatory mediators of Nfκβ and iNOS activities. Also, CAPE was found to be protective in the lung tissue and could be used as a therapeutic agent.

Caffeic Acid Phenethyl Ester Induces Vascular Endothelial Growth Factor Production and Inhibits CXCL10 Production in Human Dental Pulp Cells

“…CAPE is widely used as a health food and can be used safely. CAPE has many physiological effects such as anti-tumor, anti-inflammatory and antifungal [ 15 , 16 , 17 ]. CAPE was reported to have an inhibitory effect on tumor necrosis factor (TNF)-induced CXCL10 expression in mouse intestinal epithelial cells [ 18 ].…”