Tocotrienol-rich fraction of palm oil exhibits anti-inflammatory property by suppressing the expression of inflammatory mediators in human monocytic cells

被引:111
作者
Wu, Shu-Jing [2 ]
Liu, Po-Len [3 ]
Ng, Lean-Teik [1 ]
机构
[1] Tajen Univ, Dept Biotechnol, Pingtung, Taiwan
[2] Chia Nan Univ Pharm & Sci, Dept Hlth & Nutr, Tainan, Taiwan
[3] Kaohsiung Med Univ, Dept Resp Therapy, Kaohsiung, Taiwan
关键词
COX-2; cytokines; NF-kappa B; THP-1; cells; tocotrienols;
D O I
10.1002/mnfr.200700418
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Tocotrienol-rich fraction (TRF) of palm oil has been shown to possess potent antioxidant, anticancer, and cholesterol lowering activities. In this study, our aim was to examine the effects of TRF on LPS-induced inflammatory response through measuring the production of inflammatory mediators, namely nitric oxide (NO), prostaglandin E-2 (PGE(2)), inducible nitric oxide synthase (iNOS), cytokines (TNF-alpha, IL-4, and IL-8), cyclooxygenase-1 and -2 (COX-1 and COX-2), and nuclear factor-kappa B (NF-kappa B) in human monocytic (THP-1) cells. At concentrations 0.5-5.0 mu g/mL, TRF dose-dependently protected against LPS-induced cell death. At same concentrations, TRF also showed potent antiinflammatory activity as demonstrated by a dose-dependent inhibition of LPS (1 mu g/mL)-induced release of NO and PGF(2), and a significant decrease in the transcription of proinflammatory cytokines. TRF at 1.0 mu g/mL significantly blocked the LPS induction of iNOS and COX-2 expression, but not COX-1. This anti-inflammatory activity was further supported by the inhibition of NF-kappa B expression. These results conclude that TRF possesses potent anti-inflammatory activity, and its mechanism of action could be through the inhibition of iNOS and COX-2 production, as well as NF-kappa B expression.
引用
收藏
页码:921 / 929
页数:9
相关论文
共 57 条
[1]   Current state of therapy for pain and inflammation [J].
Abramson, SB ;
Weaver, AL .
ARTHRITIS RESEARCH & THERAPY, 2005, 7 (Suppl 4) :S1-S6
[2]   Suppression of the nuclear factor-κB activation pathway by spice-derived phytochemicals -: Reasoning for seasoning [J].
Aggarwal, BB ;
Shishodia, S .
SIGNAL TRANSDUCTION PATHWAYS, CHROMATIN STRUCTURE, AND GENE EXPRESSION MECHANISMS AS THERAPEUTIC TARGETS, 2004, 1030 :434-441
[3]   γ-tocotrienol inhibits nuclear factor-κB signaling pathway through inhibition of receptor-interacting protein and TAK1 leading to suppression of antiapoptotic gene products and Potentiation of apoptosis [J].
Ahn, Kwang Seok ;
Sethi, Gautam ;
Krishnan, Koyamangalath ;
Aggarwal, Bharat B. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2007, 282 (01) :809-820
[4]  
BAEUERLE PA, 1994, ANNU REV IMMUNOL, V12, P141, DOI 10.1146/annurev.immunol.12.1.141
[5]   Nuclear factor kappa B [J].
Barnes, PJ .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 1997, 29 (06) :867-870
[6]   NSAIDS - TIME TO REEVALUATE GUT TOXICITY [J].
BATEMAN, DN .
LANCET, 1994, 343 (8905) :1051-1052
[7]   Identities and differences in the metabolism of tocotrienols and tocopherols in HepG2 cells [J].
Birringer, M ;
Pfluger, P ;
Kluth, D ;
Landes, N ;
Brigelius-Flohé, R .
JOURNAL OF NUTRITION, 2002, 132 (10) :3113-3118
[8]   Hydrolyzed olive vegetation water in mice has anti-inflammatory activity [J].
Bitler, CM ;
Viale, TM ;
Damaj, B ;
Crea, R .
JOURNAL OF NUTRITION, 2005, 135 (06) :1475-1479
[9]  
BROUET I, 1995, BIOCHEM BIOPH RES CO, V206, P535
[10]   Salvianolic acid B attenuates VCAM-1 and ICAM-1 expression in TNF-α-treated human aortic endothelial cells [J].
Chen, YH ;
Lin, SJ ;
Ku, HH ;
Shiao, MS ;
Lin, FY ;
Chen, JW ;
Chen, YL .
JOURNAL OF CELLULAR BIOCHEMISTRY, 2001, 82 (03) :512-521