Epigallocatechin gallate diminishes cigarette smoke-induced oxidative stress, lipid peroxidation, and inflammation in human bronchial epithelial cells

Autor: Sowmya P. Lakshmi, Lakshmi Devi Kodidhela, N.Ch. Varadacharyulu, Aravind T. Reddy
Rok vydání: 2020
Předmět:
0301 basic medicine
Antioxidant
medicine.medical_treatment
Anti-Inflammatory Agents
Bronchi
Inflammation
Epigallocatechin gallate
Pharmacology
medicine.disease_cause
030226 pharmacology & pharmacy
Antioxidants
Catechin
General Biochemistry
Genetics and Molecular Biology
Cell Line
Cigarette Smoking
4-Hydroxynonenal
Proinflammatory cytokine
Lipid peroxidation
Pulmonary Disease
Chronic Obstructive
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Smoke
medicine
Humans
General Pharmacology
Toxicology and Pharmaceutics
chemistry.chemical_classification
Aldehydes
Reactive oxygen species
Chemistry
Smoking
NF-kappa B
food and beverages
Epithelial Cells
General Medicine
Pulmonary Alveoli
Oxidative Stress
030104 developmental biology
Alveolar Epithelial Cells
Lipid Peroxidation
medicine.symptom
Reactive Oxygen Species
Oxidation-Reduction
Oxidative stress
Signal Transduction
Zdroj: Life Sciences. 259:118260
ISSN: 0024-3205
DOI: 10.1016/j.lfs.2020.118260
Popis: Cigarette smoke (CS), the major risk factor of chronic obstructive pulmonary disease (COPD), contains numerous free radicals that can cause oxidative stress and exaggerated inflammatory responses in the respiratory system. Lipid peroxidation which is oxidative degradation of polyunsaturated fatty acids and results in cell damage has also been associated with COPD pathogenesis. Increased levels of lipid peroxidation as well as its end product 4-hydroxynonenal have indeed been detected in COPD patients. Additionally, reactive oxygen species such as those contained in CS can activate nuclear factor-κB signaling pathway, initiating cascades of proinflammatory mediator expression. As emerging evidence attests to the antioxidative and anti-inflammatory properties of tea catechins, we sought to determine whether epigallocatechin gallate, the most abundant tea catechin, can provide protection against oxidative stress, lipid peroxidation, and inflammatory responses caused by CS. We found that EGCG treatment blocked cigarette smoke extract (CSE)-induced oxidative stress as indicated by decreased production and accumulation of reactive oxygen species in airway epithelial cells (AECs). Likewise, lipid peroxidation in CSE-stimulated AECs was suppressed by EGCG. Our findings further suggest that EGCG sequestered 4-hydroxynonenal and interfered with its protein adduct formation. Lastly, we show that EGCG inhibited nuclear factor-κB activation and the downstream expression of proinflammatory mediators. In summary, our study describing the antioxidative and anti-inflammatory effects of EGCG in CSE-exposed AECs provide valuable information about the therapeutic potential of this tea catechin for COPD.
Databáze: OpenAIRE
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