Anti-inflammatory effects of trans-anethole in a mouse model of chronic obstructive pulmonary disease

Abstract

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 500mg/kg) 2h before intranasal challenge with 1.2 units of PPE and 7μg 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 125mg/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.