Eucalyptol, also known as 1,8-cineol, is a monoterpene and has been shown to exert anti-inflammatory and antioxidant effect. It is traditionally used to treat respiratory disorders due to its secretolytic properties. In the present study, we evaluated the effect of 1,8-cineol on pulmonary inflammation in a mouse model of acute lung injury. We found that 1,8-cineol significantly decreased the level of TNF-α and IL-1β, and increased the level of IL-10 in lung tissues after acute lung injury induced by lipopolysaccharide (LPS). It also reduced the expression of nuclear factor kappa B (NF-κB) p65 and toll-like receptor 4 (TLR4), and myeloperoxidase activity in lung tissues. In addition, 1,8-cineol reduced the amounts of inflammatory cells in bronchoalveolar lavage fluid (BALF), including neutrophils and macrophages, and significantly decreased the protein content in BALF and the lung wet/dry weight (W/D) ratio. Its effect on LPS-induced pulmonary inflammation was associated with suppression of TLR4 and NF-κB expressions. Our results provide evidence that 1,8-cineol inhibits acute pulmonary inflammation, indicating its potential for the treatment of acute lung injury.

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality, but the cellular and molecular mechanisms are still not fully understood. Type II pneumocytes are identified as the synthesizing cells of the alveolar surfactant, which has important properties in maintaining alveolar and airway stability. Lung surfactant can reduce the surface tension and prevent alveolar collapse and the airway walls collapse. Pulmonary surfactant components play important roles in normal lung function and inflammation in the lung. Surfactant has furthermore been shown to modulate the process of innate host defense, including suppression of cytokine secretion and transcription factor activation, in the inflammatory network of COPD. Abnormalities of lung surfactant might be one of the mechanisms leading to increased airway resistance in COPD. The increased expression of Granzyme A and B was found in lung tissues of patients with COPD and type II pneumocytes was proposed to be involved in the pathogenesis of COPD. These novel findings provide new sights into the role of the type II pneumocytes in the pathogenesis of COPD.

Aim: To study the effects of 1,8‐cineol (eucalyptol) on the expression of early growth response factor‐1 (Egr‐1) and NF‐κB in the human monocyte THP‐1 cell line stimulated by lipopolysaccharide (LPS). Methods: The THP‐1 cells were incubated with serial doses of 1,8‐cineol (1, 10, and 100 mg/L, 30 min) before being stimulated with LPS (1 mg/L, 30 min). The localization of Egr‐1 in the THP‐1 cells was detected by immunofluorescence and a laser scanning confocal microscope. The expression of Egr‐1 in the nuclei and whole cell, and NF‐κB in the nuclei, were measured by Western blot analysis. Results: When stimulated by LPS, the FITC‐labeled Egr‐1 was detected mainly in the nuclei. Moreover, the expression of Egr‐1 in the whole cell increased markedly compared with the control cells. 1,8‐Cineol pretreatment decreased the expression of Egr‐1 in both the nuclei and whole cell of the LPS‐stimulated THP‐1 cells, and this effect was concentration‐dependent, but there was no reaction on the expression of NF‐κB in the nuclei protein in the LPS‐stimulated THP‐1 cells. Conclusion: In a concentration‐dependent manner, 1,8‐Cineol reduces LPS‐induced Egr‐1 expression in nuclei and in whole cell of THP‐1 cells, but shows no effect on NF‐κB expression.