Protective effect of EC-18, a synthetic monoacetyldiglyceride on lung inflammation in a murine model induced by cigarette smoke and lipopolysaccharide

Highlight
• EC-18 is a synthetic monoacetyldiaglyceride (1-palmitoyl-2-linoleoyl-3-acetylglycerol).
• We investigated effects of EC-18 on lung inflammation induced by cigarette smoke and LPS in vivo.
• EC-18 reduced the inflammatory cell count and proinflammatory mediators.
• EC-18 suppressed airway inflammation and NF-κB activation.
• EC-18 may be a therapeutic agent for chronic obstructive pulmonary disease.

The antler of Sika deer (Cervus nippon Temminck) has been used a natural medicine in Korea, China and Japan, and a monoacetyldiaglyceride (1-palmitoyl-2-linoleoyl-3-acetylglycerol, PLAG) was found in the antler of Sika deer as a constituent for immunomodulation. In this study, we investigated protective effects of EC-18 (a synthetic copy of PLAG) on inflammatory responses using a cigarette smoke with lipopolysaccharide (LPS)-induced airway inflammation model. Mice were exposed to cigarette smoke for 1 h per day for 3 days. Ten micrograms of LPS dissolved in 50 μL of PBS was administered intra nasally 1 h after the final cigarette smoke exposure. EC-18 was administered by oral gavage at doses of 30 and 60 mg/kg for 3 days. EC-18 significantly reduced the number of neutrophils, reactive oxygen species production, cytokines and elastase activity in bronchoalveolar lavage fluid (BALF) compared with the cigarette smoke and LPS induced mice. Histologically, EC-18 attenuated airway inflammation with a reduction in myeloperoxidase expression in lung tissue. Additionally, EC-18 inhibited the phosphorylation of NF-κB and IκB induced by cigarette smoke and LPS exposure. Our results show that EC-18 effectively suppresses neutrophilic inflammation induced by cigarette smoke and LPS exposure. In conclusion, this study suggests that EC-18 has therapeutic potential for the treatment of chronic obstructive pulmonary disease.

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