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

Barlas, F. Baris; Erdoğan, Suat

doi:10.3906/sag-1404-14

Cited by 5 publications

(4 citation statements)

References 33 publications

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“…CAPE has been reported to suppress NO production and iNOS activity in different in vivo and in vitro models. [31][32][33]…”

Section: Discussionmentioning

confidence: 99%

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

Karaboğa¹

2018

Ulus Travma Acil Cerrahi Derg

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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.

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“…CAPE has been reported to suppress NO production and iNOS activity in different in vivo and in vitro models. [31][32][33]…”

Section: Discussionmentioning

confidence: 99%

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

Karaboğa¹

2018

Ulus Travma Acil Cerrahi Derg

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“…Its already has been demonstrated that CAPE could protect the cells from various damages such as CS or oxidative stressors. [22][23][24][25] However, the underlying mechanisms have not been sufficiently demonstrated. Although low levels of CAPE protects lung alveolar cells from damages or inflammation, higher concentrations could be apoptotic or cytotoxic.…”

Section: Discussionmentioning

confidence: 99%

“…[22] The study groups are follows: C, control (untreated); CS, tobacco cigarette smoke-exposed group; CAPE, caffeic acid phenethyl ester applied; +CAPE, CS exposed-CAPE treated cells.…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

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Küçükgül

2016

AJP

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Introduction: The main objective of this study was to evaluate the effect of antioxidative and antiapoptotic effects and underlying molecular mechanisms of caffeic acid phenethyl ester (CAPE) on human lung epithelial cells exposed to cigarette smoke (CS). Materials and Methods: Human alveolar epithelial A549 cells were exposed to CS and treated with various concentrations of CAPE for 24 h, and their effective concentrations were identified by cell viability assay (MTT). Antioxidant and anti-inflammatory effect of CAPE on nuclear erythroid related factor-2 (Nrf2) and nuclear factor-ĸβ (NF-ĸβ) protein levels were analyzed by Western blotting. Furthermore, caspase 8 gene expression level was analyzed by reverse transcription-quantitative polymerase chain reaction. Results: Low concentration CAPE pretreatment rescued 52% of CS-exposed A549 cells from death. CS upregulated gene expression level of caspase 8 by 4.28 fold. However, 2.5 µM CAPE pretreatment increased caspase 8 level by 52%. CS exposure also elevated NF-ĸβ (p65) protein level by 70%, however, CAPE pretreatment significantly reversed this activation. While CS exposure decreased Nrf2 protein levels by 48% as compared with the control group, CAPE pretreatment increased Nrf2 protein level two folds approximately according to CS group. Discussion: CAPE markedly decreased inflammatory transcription factor NF-kB and increased antioxidant response element Nrf2 protein expression levels in CS-exposed human alveolar cells. According to the data obtained from this study, CAPE could be used as a strategic alternative to support treatment of inflammatory and oxidative stress-induced lung diseases.

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“…Introduction. Among urgent problems of health care worldwide, a signifi cant place is occupied by exogenous allergic alveolitis (EAA), which attracts attention of internists and allergists and is associated with a high incidence of this pathology in the structure of allergic diseases and an increase in severe complicated forms of this disease [1][2][3][4]. Currently, EAA is regarded as the pathology, associated with the risk of disability, manifested by chronic respiratory insuffi ciency, pulmonary heart or pneumosclerosis [5].…”

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confidence: 99%

Functional Status of Prooxidant and Antioxidant Systems in the Lungs Under Experimental Allergic Alveolitis and Stress

Kovalska

2019

PSSS MS

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We have analysed the results of the study of alterations in indices of pro-oxidant (conjugated diene and malondialdehyde) and antioxidant (superoxide dismutase, ceruloplasmin, catalase) systems in guinea pigs' lungs in experimental allergic alveolitis in the dynamics of EAA development under the conditions of immobilization stress. The study included 62 female guinea pigs weighing 180-220 g, divided into 4 groups: 1 -intact guinea pigs (n=20); 2 -guinea pigs (n=14) with EAA under conditions of IS (1 st day); 3 -guinea pigs (n=14) with EAA under conditions of IS (2 nd day); 4 -guinea pigs (n=14) with EAA under conditions of IS (34 th day). The results of the experimental study showed that a signifi cant increase in conjugated diene level in animal lungs was observed at all stages of EAA development under conditions of immobilization stress as compared to a control group, indicating the activation of this marker. The same changes occurred with MDA content, indicating excessive accumulation of this lipid peroxidation product in lung tissue. Intensive synthesis of free radical compounds caused activation of some components of the enzymatic system of antioxidant defence. In particular, a moderate decrease in superoxide dismutase activity in lung tissue is observed in response to an increased level of LOPs at early stages of EAA and immobilization stress development as compared to these indices in intact animals. The same situation is observed with catalase and ceruloplasmin activity in the lungs of guinea pigs with modelled AA and IS.

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

Cited by 5 publications

References 33 publications

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

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

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Functional Status of Prooxidant and Antioxidant Systems in the Lungs Under Experimental Allergic Alveolitis and Stress

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