Caffeic acid phenethyl ester ameliorates pulmonary inflammation and apoptosis reducing Nf-κβ activation in blunt pulmonary contusion model Kafeik asit fenetil ester künt pulmoner kontüzyon modelinde pulmoner enflmasyon ve apoptozisi Nf-κβ aktivasyonunu azaltarak iyileştirir
Ulusal Travma ve Acil Cerrahi Dergisi, cilt.25, sa.5, ss.433-439, 2019 (SCI-Expanded, Scopus, TRDizin)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 25 Sayı: 5
- Basım Tarihi: 2019
- Doi Numarası: 10.5505/tjtes.2018.51694
- Dergi Adı: Ulusal Travma ve Acil Cerrahi Dergisi
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, TR DİZİN (ULAKBİM)
- Sayfa Sayıları: ss.433-439
- Anahtar Kelimeler: Apoptosis, inflammation, iNOS, Nf-kappa beta, pulmonary contusion
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- Kırklareli Üniversitesi Adresli: Hayır
Özet
BACKGROUND: Pulmonary contusion (PC) is an important life-threatening clinical condition characterized by lung injury and in-flammation. 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 sulfox-ide). 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 Nf-κβ and iNOS activities. Also, CAPE was found to be protective in the lung tissue and could be used as a therapeutic agent.