TY - JOUR
T1 - Anti-inflammatory effects of trans-anethole in a mouse model of chronic obstructive pulmonary disease
AU - Kim, Ka Young
AU - Lee, Hui Su
AU - Seol, Geun Hee
N1 - Funding Information:
This work was supported by a grant from the National Research Foundation of Korea (NRF) funded by the Korea government (MEST) (2016R1D1A1B03931081).
Publisher Copyright:
© 2017
PY - 2017/7/1
Y1 - 2017/7/1
N2 - Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that is generally characterized by progressive and irreversible airflow obstruction and alveolar destruction. Long-term treatment with current medications has been associated with various adverse effects, indicating a need for alternative approaches for the prevention and treatment of COPD. This study investigated the mechanism underlying the effects of trans-anethole in a mouse model of COPD induced by porcine pancreatic elastase (PPE) and lipopolysaccharide (LPS). BALB/c mice were orally administered trans-anethole (62.5, 125, 250, or 500 mg/kg) 2 h before intranasal challenge with 1.2 units of PPE and 7 μg of LPS. Lactate dehydrogenase (LDH) activity, cell counts, lung histology, cytokine production, and blood pressure were analyzed. Trans-anethole reduced LDH activity and inflammatory cell counts, including macrophage, neutrophil, and lymphocyte counts. trans-anethole 125 mg/kg restored the histopathological changes induced in mouse lungs by PPE and LPS. trans-anethole reduced the serum concentrations of pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), as well as significantly reducing blood pressure during chronic inflammation. Trans-anethole ameliorated chronic lung inflammation in a mouse model of COPD by reducing the serum concentrations of pro-inflammatory cytokines such as TNF-α and IL-6, and by reducing blood pressure. The present results indicate that trans-anethole may be a potential therapeutic agent for prophylaxis and treatment in patients with chronic lung inflammation.
AB - Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that is generally characterized by progressive and irreversible airflow obstruction and alveolar destruction. Long-term treatment with current medications has been associated with various adverse effects, indicating a need for alternative approaches for the prevention and treatment of COPD. This study investigated the mechanism underlying the effects of trans-anethole in a mouse model of COPD induced by porcine pancreatic elastase (PPE) and lipopolysaccharide (LPS). BALB/c mice were orally administered trans-anethole (62.5, 125, 250, or 500 mg/kg) 2 h before intranasal challenge with 1.2 units of PPE and 7 μg of LPS. Lactate dehydrogenase (LDH) activity, cell counts, lung histology, cytokine production, and blood pressure were analyzed. Trans-anethole reduced LDH activity and inflammatory cell counts, including macrophage, neutrophil, and lymphocyte counts. trans-anethole 125 mg/kg restored the histopathological changes induced in mouse lungs by PPE and LPS. trans-anethole reduced the serum concentrations of pro-inflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), as well as significantly reducing blood pressure during chronic inflammation. Trans-anethole ameliorated chronic lung inflammation in a mouse model of COPD by reducing the serum concentrations of pro-inflammatory cytokines such as TNF-α and IL-6, and by reducing blood pressure. The present results indicate that trans-anethole may be a potential therapeutic agent for prophylaxis and treatment in patients with chronic lung inflammation.
KW - Blood pressure
KW - Chronic obstructive pulmonary disease (COPD)
KW - Interleukin-6 (IL-6)
KW - Lipopolysaccharide (LPS)
KW - Porcine pancreatic elastase (PPE)
KW - Trans-anethole
UR - http://www.scopus.com/inward/record.url?scp=85019224448&partnerID=8YFLogxK
U2 - 10.1016/j.biopha.2017.05.032
DO - 10.1016/j.biopha.2017.05.032
M3 - Article
C2 - 28511344
AN - SCOPUS:85019224448
SN - 0753-3322
VL - 91
SP - 925
EP - 930
JO - Biomedicine and Pharmacotherapy
JF - Biomedicine and Pharmacotherapy
ER -