Effects of resveratrol on 12-O-tetradecanoylphorbol-13-acetate-induced oxidative events and gene expression in mouse skin

Jang, Meishiang; Pezzuto, John M.

doi:10.1016/s0304-3835(98)00250-x

Cited by 133 publications

(67 citation statements)

References 25 publications

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“…Furthermore, it has been suggested that resveratrol is one of the most potent chemopreventive agents able to block all three phases of tumor development, i.e. initiation, promotion, and progression (10), which was partly associated with the suppression of COX-2 expression and the activity of NF-κB (12,20,21). Recently, this compound also has been shown to exhibit neuroprotective effects against ß-amyloidinduced neurotoxicity in several experimental models (22,23); however, its mechanisms of action are not completely understood.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol inhibits inducible nitric oxide synthase and cyclooxygenase-2 expression in β-amyloid-treated C6 glioma cells

Kim

Lim²,

Rhee³

et al. 2006

Int J Mol Med

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Abstract.Resveratrol has been reported to exert a variety of important pharmacological effects including anti-inflammatory, cardioprotective and cancer chemopreventive properties; however, its mechanisms of action are not completely understood. ß-amyloid protein is considered to be responsible for the formation of senile plaques that accumulate in the brains of patients with Alzheimer disease. In the present study, we investigated the protective effect of resveratrol on ß-amyloid-induced cytoxicity in cultured rat astroglioma C6 cells. Preincubation of C6 cells with resveratrol concentrationdependently protected the cells from the growth inhibition induced by ß-amyloid treatment. ß-amyloid treatment led to increased nitric oxide (NO) synthesis and inducible nitric oxide synthase (iNOS) expression; however, cells pretreated with resveratrol showed a dose-dependent inhibition of NO production and iNOS expression following ß-amyloid treatment. Resveratrol also attenuated ß-amyloid-induced prostaglandin E 2 (PGE 2 ) release, which was associated with the inhibition of cyclooxygenase (COX)-2 expression. Furthermore, ß-amyloid treatment induced nuclear translocation of NF-κB, which was suppressed by resveratrol pretreatment. Collectively, the present results indicate that modulation of nuclear factor-κB (NF-κB) activity is involved in the neuroprotective action of resveratrol against ß-amyloid-induced toxicity.

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Section: Discussionmentioning

confidence: 99%

Resveratrol inhibits inducible nitric oxide synthase and cyclooxygenase-2 expression in β-amyloid-treated C6 glioma cells

Kim

Lim²,

Rhee³

et al. 2006

Int J Mol Med

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“…This antitumor effect of vitamin B6 was associated with a reduction in the incorporation of 5-bromo-2'-de -oxyuridine (BrdU) into the colonic cells (BrdU-labeling index) and the colonic expression of c-myc and c-fos proteins (oncogene products relating to cell prolifera tion), implying the involvement of reduced colonic cell proliferation in the mechanism of the effect of vitamin B6 (2). It has been reported that c-myc and c fos expres sion can be induced by oxidative stress (3,4). Since vita min B6 has been found to have a strong antioxidative ef fect (5), we postulated that the suppression effect of vi tamin B6 on the cell proliferation might be mediated * To whom correspondence should be addressed .…”

mentioning

confidence: 99%

Dietary Vitamin B6 Suppresses Colon Tumorigenesis, 8-Hydroxyguanosine, 4-Hydroxynonenal, and Inducible Nitric Oxide Synthase Protein in Azoxymethane-Treated Mice.

Komatsu

Watanabe

Oka

et al. 2002

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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SummaryRecently we reported that the supplementation of vitamin B6 to low vitamin B6 diet caused suppression in colon tumorigenesis and cell proliferation of azoxymethane treated mice in a dose-dependent manner among 1, 7, and 14mg pyridoxine HCl/kg diet (J Nutr 131: 2204(J Nutr 131: -2207(J Nutr 131: , 2001). To examine the mechanism of the anticolon tumor effect of vitamin B6, male ICR mice were fed the diet containing 1, 7, 14, and 35mg pyridoxine HCl/kg diet for 22wk and simultaneously given a weekly injection of azoxymethane for an initial 10wk. The supplementation of vitamin B6 to a low vitamin B6 diet (1mg pyridoxine HCl/kg) suppressed the levels of colonic 8-hydroxyguanosine and 4-hydroxynonenal and in ducible nitric oxide synthase protein. The results suggest that the preventive effect of vita min B6 against colon tumorigenesis is at least in part mediated by reducing oxidative stress and nitric oxide production.

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“…Thereafter, several in vivo skin cancer studies have been performed with DMBA/TPA [46,[199][200][201]235,236], DMBA alone, [237-239], TPA alone [240][241][242], ultraviolet B radiation (UVB) exposure [202][203][204]243], benzo[a]pyrene (BP) [237], and xenograft models [198]. In the DMBA/TPA models, resveratrol treatment reduced the incidence [46,[199][200][201]235], multiplicity [46,199,201,235], and tumor volume [201,235,236], and delayed the onset of tumorigenesis [201].…”

Section: Skin Cancermentioning

confidence: 99%

Chemically-Induced DNA Damage, Mutagenesis, and Cancer

2018

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Effects of resveratrol on 12-O-tetradecanoylphorbol-13-acetate-induced oxidative events and gene expression in mouse skin

Cited by 133 publications

References 25 publications

Resveratrol inhibits inducible nitric oxide synthase and cyclooxygenase-2 expression in β-amyloid-treated C6 glioma cells

Resveratrol inhibits inducible nitric oxide synthase and cyclooxygenase-2 expression in β-amyloid-treated C6 glioma cells

Dietary Vitamin B6 Suppresses Colon Tumorigenesis, 8-Hydroxyguanosine, 4-Hydroxynonenal, and Inducible Nitric Oxide Synthase Protein in Azoxymethane-Treated Mice.

Chemically-Induced DNA Damage, Mutagenesis, and Cancer

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