Biomol Ther.  2013 May;21(3):246-250.

Chitin from the Extract of Cuttlebone Induces Acute Inflammation and Enhances MMP1 Expression

Affiliations
  • 1Institute of Chronic Diseases and College of Pharmacy, Sahmyook University, Seoul 139-742, Republic of Korea. kangtj@syu.ac.kr
  • 2Department of Pharmacy, College of Pharmacy, Chungbuk National University, Cheongju 361-763, Republic of Korea. slim@chungbuk.ac.kr

Abstract

We previously reported that the extract from cuttlebone (CB) has wound healing effect in burned lesion of rat. In present study, the main component of CB extract was analyzed and its wound healing activity was evaluated by using in vitro acute inflammation model. The extract of CB stimulated macrophages to increase the production of TNF-alpha. The extract also enhanced the production of TGF-beta and VEGF, which were involved in angiogenesis and fibroblast activation. The treatment with CB extract enhanced proliferation of murine fibroblast. CB extract also induced the activation of fibroblast to increase the secretion of matrix metalloproteases 1 (MMP1). The constituent of CB extract which has wound healing activity was identified as chitin by HPLC analysis. The mechanism that the CB extract helps to promote healing of burned lesion is associated with that chitin in CB extracts stimulated wound skins to induce acute inflammation and to promoted cell proliferation and MMP expression in fibroblast. Our results suggest that CB or chitin can be a new candidate material for the treatment of skin wound such as ulcer and burn.

Keyword

Cuttlebone; Chitin; Fibroblast; Matrix Metalloprotease; Cytokine

MeSH Terms

Animals
Burns
Cell Proliferation
Chitin*
Chromatography, High Pressure Liquid
Fibroblasts
Inflammation*
Macrophages
Metalloproteases
Rats
Skin
Transforming Growth Factor beta
Tumor Necrosis Factor-alpha
Ulcer
Vascular Endothelial Growth Factor A
Wound Healing
Wounds and Injuries
Chitin
Metalloproteases
Transforming Growth Factor beta
Tumor Necrosis Factor-alpha
Vascular Endothelial Growth Factor A
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