Taipei Medical University Institutional Repository:Item 987654321/3743
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    Please use this identifier to cite or link to this item: http://libir.tmu.edu.tw/handle/987654321/3743


    Title: Dihydrolipoic acid inhibits skin tumor promotion through anti-inflammation and anti-oxidation
    Authors: 何元順
    Yuan-Soon Ho;Ching-Shu Lai;Hsin-I Liu;Sheng-Yow Ho;Chein Tai;Min-Hsiung Pan;Ying-Jan Wang
    Contributors: 醫學檢驗暨生物技術學系
    Keywords: Pharmacokinetics;Metabolism;Oxidative stress;Anticarcinogen;Lipoic acid;Oxidation;Inflammation;Antineoplastic agent;Tumor promotion;Skin;Inhibitor;Acids
    Date: 2007
    Issue Date: 2009-08-25 10:38:08 (UTC+8)
    Abstract: a-Lipoic acid (LA) has been intensely investigated as a therapeutic agent for several diseases,
    including hepatic disorder and diabetic polyneuropathy. However, the effects of LA or its
    reduced form, dihydrolipoic acid (DHLA), on cancer chemoprevention has never been
    reported. In the present study, we examined the effects of DHLA/LA on the production of
    nitric oxide (NO) by inducible NO synthase (iNOS) and the formation of prostaglandin E2
    (PGE2) by cyclooxygenase-2 (COX-2), two important mediators associated with inflammation.
    DHLA/LA significantly inhibited lipopolysaccharide (LPS)-induced NO and PGE2 formation
    in RAW 264.7 cells. Meanwhile, treatment with DHLA/LA suppressed the
    expression of iNOS protein but, unexpectedly, did not affect or increase the expression
    of COX-2 protein. The in vivo anti-inflammatory and antitumor-promoting activities were
    evaluated by a topical 12-O-tetradecanoylphorbol 13-acetate (TPA) application to mouse
    skin withmeasurement of edema formation, epidermal thickness and hydrogen peroxide
    production. DHLA significantly inhibited the priming and activation stages of skin inflammation
    induced by a double TPA application, by decreasing the inflammatory parameters.
    Furthermore, DHLA inhibited DMBA (0.3 mmol)/TPA (2.0 nmol)-induced skin tumor formation
    by reducing the tumor incidence and tumor multiplicity. When applied topically
    onto the shaven backs of mice prior to TPA, DHLA markedly inhibited the expression of
    iNOS protein. DHLA also strongly and directly inhibited COX-2 activity. These results
    suggest that DHLA can be a possible chemopreventive agent in inflammation-associated
    tumorigenesis.
    alpha-Lipoic acid (LA) has been intensely investigated as a therapeutic agent for several diseases, including hepatic disorder and diabetic polyneuropathy. However, the effects of LA or its reduced form, dihydrolipoic acid (DHLA), on cancer chemoprevention has never been reported. In the present study, we examined the effects of DHLA/LA on the production of nitric oxide (NO) by inducible NO synthase (iNOS) and the formation of prostaglandin E2 (PGE(2)) by cyclooxygenase-2 (COX-2), two important mediators associated with inflammation. DHLA/LA significantly inhibited lipopolysaccharide (LPS)-induced NO and PGE(2) formation in RAW 264.7 cells. Meanwhile, treatment with DHLA/LA suppressed the expression of iNOS protein but, unexpectedly, did not affect or increase the expression of COX-2 protein. The in vivo anti-inflammatory and antitumor-promoting activities were evaluated by a topical 12-O-tetradecanoylphorbol 13-acetate (TPA) application to mouse skin with measurement of edema formation, epidermal thickness and hydrogen peroxide production. DHLA significantly inhibited the priming and activation stages of skin inflammation induced by a double TPA application, by decreasing the inflammatory parameters. Furthermore, DHLA inhibited DMBA (0.3 micromol)/TPA (2.0 nmol)-induced skin tumor formation by reducing the tumor incidence and tumor multiplicity. When applied topically onto the shaven backs of mice prior to TPA, DHLA markedly inhibited the expression of iNOS protein. DHLA also strongly and directly inhibited COX-2 activity. These results suggest that DHLA can be a possible chemopreventive agent in inflammation-associated tumorigenesis.
    Relation: Biochemical Pharmacology.(73):1786-1795.
    Data Type: article
    Appears in Collections:[ ] Periodical Articles

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