Triterpene Acids of Loquat Leaf Improve Inflammation in Cigarette Smoking Induced COPD by Regulating AMPK/Nrf2 and NFκB Pathways
Autor: | Yuexian Wu, Jing Li, Weilin Li, Jian Chen, Tunyu Jian, Bingru Ren, Jiawei Li, Xiaoqin Ding, Han Lv |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Male triterpene acids AMPK Nitric Oxide Synthase Type II Pharmacology AMP-Activated Protein Kinases chemistry.chemical_compound Pulmonary Disease Chronic Obstructive 0302 clinical medicine Lung COPD Nutrition and Dietetics biology cigarette smoke NF-kappa B Malondialdehyde Nitric oxide synthase iNOS Keywords loquat leaf 030220 oncology & carcinogenesis loquat leaf Phosphorylation Cytokines medicine.symptom Inflammation Mediators lcsh:Nutrition. Foods and food supply Signal Transduction NF-E2-Related Factor 2 Inflammation lcsh:TX341-641 Article Nrf2 Cigarette Smoking chronic obstructive pulmonary disease Superoxide dismutase 03 medical and health sciences Weight Loss medicine Animals Protein kinase A business.industry Body Weight medicine.disease Triterpenes Mice Inbred C57BL Plant Leaves Oxidative Stress 030104 developmental biology Eriobotrya chemistry inflammation biology.protein business Food Science NFκB |
Zdroj: | Nutrients Volume 12 Issue 3 Nutrients, Vol 12, Iss 3, p 657 (2020) |
ISSN: | 2072-6643 |
DOI: | 10.3390/nu12030657 |
Popis: | 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 1&beta (IL-1&beta ), IL-2, IL-6, and tumor necrosis factor &alpha (TNF-&alpha ). 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 (NF&kappa B) 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 NF&kappa B pathways. Our findings suggest that TAs could be considered as a promising functional material for treating CS-induced COPD. |
Databáze: | OpenAIRE |
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