Caffeic acid phenethyl ester protects lung alveolar epithelial cellsfrom cigarette smoke-induced damage

FIRAT BARIŞ BARLAS; SUAT ERDOGAN

Article Details

Caffeic acid phenethyl ester protects lung alveolar epithelial cellsfrom cigarette smoke-induced damage

Authors:

FIRAT BARIŞ BARLAS | SUAT ERDOGAN

Publisher:

TUBITAK

Journal:

Turkish Journal of Medical Sciences 2015 Vol.45 Issue 3, pp.534-541

Document Type:

Article

Publication Date:

8/2015

Document Language:

Turkish

Document ID (Org No.):

2000752654

Frequency:

Bimonthly

eISSN:

1303-6165

pISSN:

1300-0144

Keywords:

Abstract:

 

Background/aim: To evaluate the influence of caffeic acid phenethyl ester (CAPE) on cigarette smoke (CS)-induced cell damage, oxidative stress, and inflammation in human alveolar epithelial cells.   Materials and methods: A549 alveolar epithelial cells were divided into control, CS exposure, CAPE, and CS+CAPE treatment groups. Undiluted CS-exposed medium (100%) and three dilutions (50%, 25%, and 10%) of CS-exposed media were applied to cultured A549 cells, which were analyzed after 3 h of incubation. Viability was measured by MTT assay, the gene expressions were evaluated by real-time PCR, and spectrophotometric techniques were used for biochemical assessments.   Results: While CS exposure markedly reduced cellular viability by 32% after 3 h of incubation, 2.5 µM CAPE treatments prevented CS-induced cell death by 40% in the cells. CS exposure triggered lipid peroxidation and depleted antioxidant capacity through inhibiting catalase activity and depleting glutathione levels. Moreover, CS increased nitric oxide production via upregulation of iNOS expression. CAPE treatment significantly restored antioxidant capacity and prevented lipid peroxidation. Cigarette smoke exposure induced inflammation by significantly upregulating TNF-?, IL-1Ã, and COX-2 mRNA expressions (3-, 2- and 25-fold, respectively). CAPE treatment of A549 cells significantly reversed the inflammation.   Conclusion: CAPE may potentially represent a new therapeutic option in the prevention of CS-induced lung damages.

 

Background/aim: To evaluate the influence of caffeic acid phenethyl ester (CAPE) on cigarette smoke (CS)-induced cell damage, oxidative stress, and inflammation in human alveolar epithelial cells.   Materials and methods: A549 alveolar epithelial cells were divided into control, CS exposure, CAPE, and CS+CAPE treatment groups. Undiluted CS-exposed medium (100%) and three dilutions (50%, 25%, and 10%) of CS-exposed media were applied to cultured A549 cells, which were analyzed after 3 h of incubation. Viability was measured by MTT assay, the gene expressions were evaluated by real-time PCR, and spectrophotometric techniques were used for biochemical assessments.   Results: While CS exposure markedly reduced cellular viability by 32% after 3 h of incubation, 2.5 µM CAPE treatments prevented CS-induced cell death by 40% in the cells. CS exposure triggered lipid peroxidation and depleted antioxidant capacity through inhibiting catalase activity and depleting glutathione levels. Moreover, CS increased nitric oxide production via upregulation of iNOS expression. CAPE treatment significantly restored antioxidant capacity and prevented lipid peroxidation. Cigarette smoke exposure induced inflammation by significantly upregulating TNF-?, IL-1Ã, and COX-2 mRNA expressions (3-, 2- and 25-fold, respectively). CAPE treatment of A549 cells significantly reversed the inflammation.   Conclusion: CAPE may potentially represent a new therapeutic option in the prevention of CS-induced lung damages.

Article Details

Caffeic acid phenethyl ester protects lung alveolar epithelial cellsfrom cigarette smoke-induced damage

Authors: FIRAT BARIŞ BARLAS | SUAT ERDOGAN

Publisher: TUBITAK

Journal: Turkish Journal of Medical Sciences 2015 Vol.45 Issue 3, pp.534-541

Document Type: Article

Publication Date: 8/2015

Document Language: Turkish

Document ID (Org No.): 2000752654

Frequency: Bimonthly

eISSN: 1303-6165

pISSN: 1300-0144

Caffeic acid phenethyl ester

CAPE

inflammation

oxidative stress

cigarette smoke

A549

Issues

Authors:

FIRAT BARIŞ BARLAS | SUAT ERDOGAN

Publisher:

TUBITAK

Journal:

Turkish Journal of Medical Sciences 2015 Vol.45 Issue 3, pp.534-541

Document Type:

Article

Publication Date:

8/2015

Document Language:

Turkish

Document ID (Org No.):

2000752654

Frequency:

Bimonthly

eISSN:

1303-6165

pISSN:

1300-0144