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Anti‐inflammatory, Anti‐proliferative Activities from the Skin of the Catfish Arius Bilineatus, Valenciennes
Author(s) -
Yang Peiying,
Ding Jibin,
Tang Lin,
Rhea Patrea,
Pan Yong,
Afzal Mohammad,
Paul Bincy Maniyalil,
Oommen Sosamma,
AlHassan Jassim M.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.612.6
Subject(s) - catfish , arachidonic acid , anti inflammatory , chemistry , in vitro , mtt assay , inflammation , pharmacology , a549 cell , biochemistry , biology , immunology , enzyme , fish <actinopterygii> , fishery
The catfish secretes a gelatinous substance composed of biochemically active lipids and proteins from its skin upon stress or injury. Preparations from the skin have previously been shown to affect blood clotting and accelerates healing of non‐healing diabetic foot ulcers in man. Here catfish skin preparation (CSP) and its lipid fraction were investigated with the focus on its ability to alter key inflammatory mediators and to inhibit the proliferation of human non‐small cell lung cancer (NSCLC) A549 cells and human hepatocellular carcinoma Hep3B cells. The anti‐inflammatory activity was determined by its effect on arachidonate metabolism in cells in vitro or in mouse ear tissues by LC/MS/MS method, and on the inflammatory genes analyzed by inflammation array kits (PCR based). The antiproliferative activity of CSP was evaluated by MTT assay. When A549 cells were treated with CSP or different lipid fraction of CSP (200 μg/ml), total lipid fraction noticeably reduced the cellular level of PGE 2 by 64.2%, whereas the petroleum either fraction of CSP decreased the production of PGI 2 , TEXB 2 , PGF 2α , PGE 2 and PGE 1 by 42%, 24%, 76%, 55% and 68%, respectively compared to that of control vehicle treated cells. Similarly, chloroform fraction of CSP also reduced the cellular level of PGI 2 and PGF 2α by 67% and 74%, respectively in A549 cells. To further identify the anti‐inflammatory properties of CSP, we then tested the anti‐inflammatory effect of CSP in arachidonic acid induced mouse ear model. Intriguingly, the cream prepared from the total lipid CSP (10 mg) reduced the redness of ears caused by arachidonic acid, and significantly reduced mouse ear weight (p < 0.05) suggesting anti‐inflammatory activity of the CSP. Analyzing mouse ear eicosanoid levels revealed that PGE 2 was reduced by 28% as well as 5‐lipoxygenase metabolite 5‐HETE by 30% in the CSP cream treated group compared to that of control group. The inflammatory genes were further tested in the control and CSP cream treated mouse ear tissues. Intriguingly, the LTA4 hydrolase gene which is downstream of 5‐LOX and responsible for formation of pro‐inflammatory mediator LTB4 was reduced by 50%. Given inflammation is one of the key factors associated with tumor development, we then tested the anti‐proliferative activities of the total lipid extract and its lipid fractions in A549 cells and Hep3B cells. The growth of both A549 and Hep3B cells was significantly inhibited by chloroform fraction of CSP with IC 50 around 25 mg/ml. Together, these data suggest that CSP and its lipid soluble fraction have both anti‐inflammatory and anti‐proliferative activities which may be mediated through alteration of arachidonate metabolism and warrants further investigation. Support or Funding Information This study was support by a grant from Kuwait Foundation for the Advancement of Science No. KFAS 201320701A‐D, and Kuwait University Research Grant No. SL03/14.