Caffeic acid phenethyl ester ameliorates pulmonary inflammation and apoptosis reducing Nf-κβ activation in blunt pulmonary contusion model

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 Nf-κβ and iNOS activities. Also, CAPE was found to be protective in the lung tissue and could be used as a therapeutic agent.

Kafeik asit fenetil ester künt pulmoner kontüzyon modelinde pulmoner enflmasyon ve apoptozisi Nf-κβ aktivasyonunu azaltarak iyileþtirir

AMAÇ: Pulmoner kontüzyon (PC), akciðer hasarý ve enflamasyon ile karakterize, hayatý tehdit eden önemli bir klinik durumdur. Kafeik asit fenetil ester (CAPE), güçlü antioksidan ve anti-enflamatuvar etkileri olan biyolojik bir ajandýr. Bu çalýþmada, CAPE’nin deneysel PC modelinde doku hasarý, nükleer faktör kappa-beta (Nf-κβ) aktivitesi, indüklenebilir nitrik oksit sentaz (iNOS) sentezi ve pulmoner apoptozis üzerindeki etkileri araþtýrýldý.
GEREÇ VE YÖNTEM: Çalýþmada 40 yetiþkin Wistar albino sýçaný kullanýldý ve dört gruba ayrýldý: Kontrol, PC, PC + CAPE ve CAPE. CAPE, PC oluþumunu takiben yedi gün boyunca intraperitonal olarak uygulandý (dimetil sülfoksit içinde çözülmüþ 10 umol/kg). Akciðer dokusunda ýslak/kuru aðýrlýk oraný belirlendi. Pulmoner doku hematoksilen-eosin ve masson trikrom histokimyasal boyamasý ile ve taramalý elektron mikroskobu ile incelendi. Akciðerlerdeki Nf-κβ ve iNOS aktiviteleri indirekt immünhistokimyasal yöntemle belirlendi. Pulmoner apoptozis, TUNEL yöntemi ile tespit edildi.
BULGULAR: Pulmoner kontüzyon grubunda artmýþ lökosit infiltrasyon skoru, pulmoner ödem, alveoler hasar ve artmýþ Nf-κβ ve iNOS aktiviteleri tespit edildi. CAPE uygulamasý Nf-κβ ve iNOS aktivitelerini ve pulmoner apoptozu azaltmaktadýr.
TARTIÞMA: Çalýþmanýn sonuçlarý, CAPE’nin Nf-κβ ve iNOS enflamatuvar mediatörlerini baskýlayarak doku hasarýný engellediðini ettiðini açýkça göstermektedir. Ayrýca, CAPE’nin akciðer dokusunda koruyucu olduðunu ve terapötik bir ajan olarak kullanýlabileceðini göstermektedir.