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
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