Cigarette smoking (CS) is believed to be an important inducement in the pathological development of chronic obstructive pulmonary disease (COPD), a progressive lung disease. Loquat is an Asian evergreen tree commonly cultivated for its fruit. Its leaf has long been used as an important material for both functional and medicinal applications in the treatment of lung disease in China and Japan. As the principal functional components of loquat leaf, triterpene acids (TAs) have shown notable anti-inflammatory activity. However, their protective activity and underlying action of mechanism on CS-induced COPD inflammation are not yet well understood. In the present study, male C57BL/6 mice were challenged with CS for 12 weeks, and from the seventh week of CS exposure, mice were fed with TAs (50 and 100 mg/kg) for 6 weeks to figure out the therapeutic effect and molecular mechanism of TAs in CS-induced COPD inflammation. The results demonstrate that TA suppressed the lung histological changes in CS-exposed mice, as evidenced by the diminished generation of pro-inflammatory cytokines, including interleukin 1β (IL-1β), IL-2, IL-6, and tumor necrosis factor α (TNF-α). Moreover, TA treatment significantly inhibited the malondialdehyde (MDA) level and increased superoxide dismutase (SOD) activity. In addition, TAs increased the phosphorylation of AMP-activated protein kinase (AMPK) and nuclear factor erythroid-2-related factor-2 (Nrf2) expression level, while inhibiting phosphorylation of nuclear factor kappa B (NFκB) and inducible nitric oxide synthase (iNOS) expression in CS-induced COPD. In summary, our study reveals a protective effect and putative mechanism of TA action involving the inhibition of inflammation by regulating AMPK/Nrf2 and NFκB pathways. Our findings suggest that TAs could be considered as a promising functional material for treating CS-induced COPD.
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http://dx.doi.org/10.3390/nu12030657 | DOI Listing |
Curr Res Toxicol
December 2024
Department of Biomechatronics Engineering, National Taiwan University, No. 1, Sec. 4, Roosevelt Road, Taipei 10617, Taiwan.
Current treatments for chronic obstructive pulmonary disease (COPD), a common respiratory condition, include oxygen therapy and steroids for temporary relief. In this study, we established a rat model of cigarette smoke (CS)-induced COPD and investigated the benefits of a hydrogen-oxygen generator in this model. CS-exposed rats were treated using either a hydrogen-oxygen generator or a steroid.
View Article and Find Full Text PDFMol Ther
January 2025
Immune Health, Hunter Medical Research Institute and The University of Newcastle, Newcastle, New South Wales, Australia; Centre for Inflammation, Centenary Institute and University of Technology Sydney, School of Life Sciences, Faculty of Science, Sydney, New South Wales, Australia. Electronic address:
Vitronectin (VTN) is an important extracellular matrix protein in tissue remodeling, but its role in COPD is unknown. We show that VTN regulates tissue remodeling through urokinase plasminogen activator (uPA) signaling pathway in COPD. In human COPD airways and bronchoepithelial cells and the airways of mice with cigarette smoke (CS)-induced experimental COPD, VTN protein was not changed, but downstream uPA signaling was altered (increased plasminogen activator inhibitor-1, uPAR) that induced collagen and airway remodeling.
View Article and Find Full Text PDFSci Rep
December 2024
State Key Laboratory of Biobased Material and Green Papermaking, School of Bioengineering, Qilu University of Technology, Shandong Academy of Sciences, Jinan, People's Republic of China.
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide, characterized by persistent respiratory symptoms and airflow limitations resulting from small airway injury, bronchial wall thickening, and hypersecretion of mucus. Current pharmacological interventions are ineffective in reversing these airflow limitations; In our study, we investigated the potential role of patchouli essential oil (PEO) in the treatment of COPD and its underlying molecular mechanisms, both in vitro and in vivo. To establish a cigarette smoke-induced COPD mice model, we exposed the mice to cigarette smoke (CS) and administered nasal drip of lipopolysaccharides (LPS).
View Article and Find Full Text PDFFront Vet Sci
December 2024
Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Background: The effects of camel milk in inflammation and systemic oxidative stress of cigarette smoke (CS)-induced chronic obstructive pulmonary disease (COPD) associated with small airway inflammation in rats were investigated.
Methods: 35 male Wistar rats were randomly divided into five groups: (a) control, (b) CS-exposed rats, c and (d) CS-exposed rats treated with the 4 and 8 mL/kg camel milk, and (e) CS-exposed rats treated with 1 mg/kg dexamethasone.
Results: Total and differential WBC counts, serum level of TNF- and malondialdehyde (MDA) level in serum and homogenized tissues of the heart, kidney, liver, and testicle were significantly increased, but catalase (CAT), superoxide dismutase (SOD) and thiol levels were significantly decreased in CS-exposed rats ( < 0.
Respir Res
December 2024
Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, No.36 Sanhao Street, Shenyang, 110004, Liaoning, China.
Background: Alveolar macrophages (AMs) modulate pulmonary inflammation in chronic obstructive pulmonary disease (COPD), contributing to its progression. The PPARγ/RXRα heterodimer influences AM polarization induced by cigarette smoke (CS). Although PPARγ agonists suppress CS-induced M1 macrophage polarization, the impact of RXRα agonists on this process has not been determined.
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