Cigarette smoke exposure is the major cause of chronic obstructive pulmonary disease (COPD). Acetylshikonin was the active principle component of Purple Gromwell that show anti-oxidative and anti-inflammatory effect. However, no data are available to elucidate the protective effect of acetylshikonin on COPD. Acetylshikonin could attenuate smoke-induced lung pathological changes, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), and monocyte chemoattractant protein 1 (MCP-1) productions, and tissue damages caused by oxidative stress. Furthermore, acetylshikonin was found to enhance the expression of Nrf2 and Nur77-mediated COX-2 in vivo and in vitro.
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http://dx.doi.org/10.1080/10286020.2019.1694512 | DOI Listing |
Front Pharmacol
December 2024
China National Tobacco Quality Supervision & Test Center, Zhengzhou, China.
Sci 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 PDFImmun Inflamm Dis
December 2024
Department of Xinjiang Laboratory of Respiratory Disease Research, Traditional Chinese Medicine Hospital Affiliated to Xinjiang Medical University, Urumqi, Xinjiang, China.
Background: Chronic obstructive pulmonary disease (COPD), a prevalent respiratory condition, is characterized by long-term airway inflammation, which can lead to airway remodeling and persistent airflow restriction. Exposure to cigarette smoke is known as a major contributor to COPD development. Research has confirmed that ferroptosis and m6A modification are closely related to various inflammatory-related diseases.
View Article and Find Full Text PDFIntroduction: The incidence of chronic obstructive pulmonary disease (COPD) appears to be increasing and evidence suggests that the intestinal flora may play a causative role in its development. Previous studies found that the Shenqi Wenfei Formula (SQWF) can regulate pyroptosis via the NLRP3/GSDMD pathway, thereby reducing the inflammatory response in the lungs of COPD model rats. However, there is no information on whether the drug's effects are associated with intestinal flora.
View Article and Find Full Text PDFLung
December 2024
State Key Laboratory of Biotherapy of China, Division of Pulmonary Diseases, Department of Pulmonary and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, 610041, China.
Purpose: This study investigated the efficacy and underlying mechanism of the mitochondrial fusion promoter M1 in mitigating cigarette smoking (CS)-induced airway inflammation and oxidative stress both in vitro and in vivo models.
Methods: Cigarette smoke extract (CSE)-treated airway epithelial cells (BEAS-2B) and CS-exposed mice were pretreated with M1, followed by the measurement of proinflammatory cytokines, oxidative stress, mitochondrial fusion proteins (MFN2 and OPA1) and fission proteins (DRP1 and MFF). Molecular pathways were elucidated through transcriptomic analysis and Western blotting.
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