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

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

  • Int Immunopharmacol. 2016 Jan:30:62-68. doi: 10.1016/j.intimp.2015.11.025.
In-Sik Shin 1 Kyung-Seop Ahn 2 Na-Rae Shin 2 Hyun-Jun Lee 2 Hyung Won Ryu 2 Jae Wha Kim 3 Ki-Young Sohn 4 Heung Jae Kim 4 Yong-Hae Han 4 Sei-Ryang Oh 5
Affiliations

Affiliations

  • 1 Veterinary Pharmacology, College of Veterinary Medicine, Chonnam National University, 77, Yongbong-ro, Buk-gu, Gwangju 500-757, Republic of Korea.
  • 2 Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, 30 Yeongudanji-ro, Ochang-eup, Cheongju, Chungbuk 363-883, Republic of Korea.
  • 3 Medical Genomics Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 125, Republic of Korea.
  • 4 ENZYCHEM Lifesciences, 103-6, KAIST-ICC F741, Munjidong, Daejeon 305-732, Republic of Korea.
  • 5 Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, 30 Yeongudanji-ro, Ochang-eup, Cheongju, Chungbuk 363-883, Republic of Korea. Electronic address: [email protected].
Abstract

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 1h per day for 3days. Ten micrograms of LPS dissolved in 50μL of PBS was administered intra nasally 1h after the final cigarette smoke exposure. EC-18 was administered by oral gavage at doses of 30 and 60mg/kg for 3days. 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.

Keywords

Chronic obstructive pulmonary disease; Cigarette smoke; EC-18; Lung inflammation; Monoacetyldiaglyceride.

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